Quiz 2 Flashcards

1
Q

Physiology of Coagulation

A

Ultimate goal: Hemostasis

Physiologic process by which bleeding is stopped:

  1. Formation of a platelet plug
  2. 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)

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2
Q

Platelet Aggregation ( platelet plug formation)

A
  1. platelets come in contact with collagen on the exposed surface of a damaged vessel- adhere to the site- platelet activation is initiated.
  2. Platelet activation leads to platelet aggregation
  3. Platelet aggregation ends with formation of fibrinogen bridges between glycoprotein IIb/IIIa receptors on adjacent platelets

BLOOD CLOT!

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3
Q

Indications for Anticoagulants

A
  1. DVT
  2. Atherosclerosis
  3. Stroke
  4. Acute Coronary Syndrome
    - Unstable angina, MI
  5. PVD
  6. Oncologic Processes
  7. Genetic Predisposition
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4
Q

Lab Values

A
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

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5
Q

Pharmacotherapeutics of Anticoagulants

A

Interrupt clotting cascade
Do NOT break down existing clots

Given IV, SQ, or PO

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6
Q

Pharmacotherapeutics of Anti-platelet agents

A

interfere with platelet membrane function and platelet aggregation

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7
Q

Pharmacotherapeutics of Thrombolytics

A

Lyse ( dissolve ) existing clots

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8
Q

Heparin

A

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

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9
Q

Enoxaprin ( Lovanox)

A

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

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10
Q

Warfarin

A

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)

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11
Q

Direct Thrombin Inhibitors

Think GATOR

A

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

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12
Q

Rivaroxaban (Xarelto)

A

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

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13
Q

Asprin

A

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

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14
Q

clopidogrel bisulfate(Plavix)

A

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

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15
Q

recombinant alteplase

dugs that end in - ASE

A

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
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16
Q

Antihemophilic Factor (Factor VIII)

A

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.

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17
Q

(Amicar) aminocaproic acid

A
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

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18
Q

Blood pressure

A

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

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19
Q

Primary HTN

A

(Essential) Hypertension

-No identifiable cause

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20
Q

Secondary Hypertension

A
Identifiable causes:
Renal disease
Oral contraceptive use
Reno-vascular disease
Cushings syndrome
Pheochromocytoma ( tumor of adrenal gland)
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21
Q

Consequences of HTN

A
  • 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

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22
Q

Benefits of lowering BP

A

Decrease in:

morbidity
strokes
MI
Heart failure

Increase in LIFESPAN

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23
Q

Evaluate HTN patients for

A

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

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24
Q

Therapeutic intervnetions

A

Lifestyle changes

Antihypertensive drug therapy

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25
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
26
Classes of Hypertensive Drugs
1. Diuretics 2. 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 ```
27
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
28
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
29
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
30
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 ```
31
Labetolol:
Alpha/Beta Blocker Blocks beta 1 and beta 2 and selective alpha 1 Alpha blocking cause peripheral vasodilation Beta blocking prevents reflex tachycardia
32
Centrally Acting Alpha Agonists
( -DINE) | -DOPA
33
Clonidine (Catapres)
MOA: Inhibits sympathetic nervous system response and reduces sympathetic outflow from the CNS ↓ HR, BP, vasoconstriction and vascular resistance Severe rebound HTN if discontinued
34
Methyldopa (Aldomet)
- Displaces norepinephrine from storage sites | - Drug of choice for pregnant women with HTN
35
Drugs that act on RAAS
``` Angiotensin I (naturally causes): Little biologic activity ``` Angiotensin II (naturally causes): - Vasoconstriction - Release of aldosterone - Alteration of cardiac and -vascular structure Renin (naturally causes): -Catalyzes the formation of Angiotensin I -Released in response to decreased BP, blood volume, plasma sodium content, or renal perfusion pressure Angiotensin-Converting Enzyme (ACE) - Located on luminal surface of blood vessels - Catalyzes angiotensin I to angiotensin II **ACE can act on other substrates so it is also known as bradykinin RAAS- Regulates BP! -Vasoconstriction ( within minutes -hours) -Renal Water retention ( vasoconstriction decreases GFR; Stimulate release of Aldosterone) aldosterone- RETAINS NA+ and water
36
ACE Inhibitors ( -PRIL)
MOA: Suppress formation of angiotensin II - Dilate blood vessels - Reduce blood volume - Prevent or reverse pathologic changes in the heart and blood vessels mediated by angiotensin II and aldosterone ``` Therapeutic Uses: HTN Heart failure MI Diabetic and non diabetic nephropathy Prevention of MI, stroke, and death in patients with high CV risk Diabetic retinopathy ``` ``` Significant adverse effects: #1 persistent dry Cough -Hyperkalemia -First dose hypotension -Renal failure -Angioedema ``` ACE Inhibitors contraindicated in 2nd and 3rd trimesters Drug Interactions: - Diuretics - Antihypertensive agents - Drugs that raise potassium levels - Lithium - NSAIDs Administration- PO without regard to meal
37
Enalprilat
Only ACE inhibitor give in IV form
38
ARBs ( Angiotensin II Receptor Antagonists | SARTAN
MOA: Prevents angiotensin II from binding to receptors in many tissues, thus blocking the vasoconstricting and aldosterone-secreting effects of angiotensin II -Decreases peripheral vascular resistance Does not cause” ACE cough” or hyperkalemia ``` Therapeutic Uses: HTN Heart failure MI Diabetic nephropathy Stroke prevention Prevention of MI, stroke, and death in patients with high CV risk Diabetic retinopathy ``` Adverse Effects: - Angioedema - ARB’s contraindicated in 2nd and 3rd trimesters - Renal failure Administration: Available PO and can be administered with or without food
39
Calcium Channel Blockers
-Antagonists MOA:Prevent calcium from entering the cells Treatment of : HTN, angina, and cardiac dysrhythmias Examples: *Verapamil (Calan) Blocks Ca channels in blood vessels and in the heart *Diltiazem (Cardizem) Inhibits calcium ion influx, reduce afterload ``` Direct effects: ↓arterial pressure ↓HR ↓AV nodal conduction ↓force of contraction ↑coronary perfusion Reflex responses ``` Indirect effects: Barroreceptor activated Increased firing of sympathetic nerves to the heart Direct and indirect negate each other Drug interactions with Beta blockers
40
Nifedipine (ProcardiaXL, Adalat)
Inhibits calcium ion influx -Vasodilating effects on coronary and peripheral arterioles -Does not slow AV node conduction but can cause cardiosuppression in toxic doses Used for angina and HTN Adverse effects : Flushing Dizziness Reflex tachycardia Common adverse effects for oral preparations: GI: constipation, nausea CV: HA dizziness Monitor and treat adverse effects supportively Overdose: IV calcium chloride or calcium gluconate
41
Direct Acting Vasodilators
Hydralazine (Apresoline) MOA: ↓Peripheral resistance Adjunct with other antihypertensives Adverse effect: -Lupus like syndrome -Reflex tachycardia Combined with beta blockers or clonidine to prevent reflex tachycardia from vasodilation -Fluid retention Combined with a diuretic to offset fluid retention from ↑ production of angiotensin II Drug Interactions: Beta blockers
42
Direct Acting Vasodilators
Nitroprusside (Nitropress) ``` Used to treat: hypertensive crisis (DBP>120) ``` MOA:Directly relaxes vascular smooth muscle, Dilates veins more than arteries ↓ preload and afterload ↓ BP dramatically IV use only MUST use a pump Protect from light Monitor BP
43
Adrenergic Agonist Epinephrine ( used in SHOCK)
Nonselective adrenergic agonist: Stimulates all alpha and beta receptors ``` Many therapeutic uses, such as: Cardiopulmonary arrest Ventricular fibrillation Anaphylactic shock Asthma ``` Adverse effects: stimulation of all receptors are common. CNS and cardiac adverse effects are the most common and may be the most serious.
44
Adrenergic Agonists | Dopamine
Catecholamine and a precursor to NE - Vasopressor used in treating shock - IV administration only in acute care settings - Invasive monitoring, pump Adverse effects: CV system effects - Stimulation of alpha-1, beta-1 and dopamine receptors is dose dependent - Weight based dosing IMPORTANT Correct hypovolemia first Contraindications: Pheochromocytoma Uncorrected tachyarrhythmias V-fib
45
Adrenergic Agonist | phenylephrine (NeoSynephrine IV)
Alpha-1 stimulant Potent vasoconstrictor Avoid IV extravasation Pharmacotherapeutics include: Vascular failure Hypotension Shock states Topical pharmacotherapeutics: - Nasal decongestant (sudafed) - Pupil dilation (mydriasis)
46
Adrenergic Agonist | Isoproterenol
Nonselective beta-2 stimulant. Pharmacotherapeutics include: Congestive heart failure Various types of shock Hypoperfusion ``` Inhaled pharmacotherapeutics include: Asthma Bronchitis Emphysema Adverse effects are primarily related to cardiac stimulation ```
47
Heart Failure
Heart is unable to pump sufficient blood to meet the metabolic demands of the tissues KEY: Not every patient has signs of systemic or pulmonary congestion ``` Can be: Progressive Ventricular dysfunction Reduced CO Insufficient tissue perfusion Signs of fluid retention ``` ``` Causes: Chronic HTN MI Coronary Artery Disease Valvular disease Congenital heart disease Dysrhythmias Aging myocardium ```
48
Cardiac remodeling( BAD BAD BAD)
Physiologic adaptations to reduced cardiac output ``` Cardiac dilation ↑ sympathetic tone ↑ HR, ↑ contractility, ↑ venous tone, ↑ arteriolar tone H20 retention and ↑ blood volume Natriuretic peptides ```
49
SXS of Heart Failure
``` ↓ exercise tolerance Fatigue SOB Tachycardia Cardiomegaly Pulmonary edema Peripheral edema hepatomegaly JVD Weight gain – fluid retention ```
50
Stages of Heart Failure ( AHA)
Stage A -No symptoms, no structural or functional cardiac abnormalities -Do have associated behaviors HTN, CAD, Diabetes Stage B- No S/S but do have structural heart disease LV hypertrophy or fibrosis, LV dilation Stage C- Symptoms and structural heart disease Stage D- Advanced structural disease and severe symptoms
51
How do you treat heart failure
Diuretics - Thiazide diuretics - Loop diuretics - Potassium sparing diuretics ACE Inhibitors/ARBs: - Dilate arterioles - Dilate veins - Decrease release of aldosterone - Favorable effects on cardiac remodeling ``` Adverse effects on heart: Hypotension Hyperkalemia Intractable cough Angioedema ``` ***Diovan******* Only ARB approved for treating HF Similar to ACE without effects on cardiac remodeling ``` Beta Blockers: Carvedilol, metoprolol -Improve LV ejection fraction -protect the heart from excessive sympathetic stimulation -protect the heart from dysrhythmias -Increase exercise tolerance -Slow progression of heart failure ``` ``` ****Start doses low*** Adverse effects on heart: Fluid retention and worsening heart failure Fatigue Hypotension Bradycardia or heart block ```
52
Digoxin for Heart Failure
Digoxin ( Cardiac Glycoside) Positive inotrope Inhibits sodium, potassium-ATPase → promotes calcium accumulation → augmentation of contractile force Potassium competes with dig for binding to sodium, potassium-ATPase → when potassium is low there is ↑dig binding → digoxin toxicity ↑ potassium there is inhibition of sodium, potassium-ATPase ↓ therapeutic response of digoxin ``` Benefits in Heart Failure: Increased cardiac output Decreased sympathetic tone Decreased heart rate Decreased afterload Reduced venous pressure Increased urine output ``` Narrow therapeutic window .5 - 2.0 Renal excretion ``` Adverse effects: Dysrhythmias Digoxin-induced dysrhythmias Noncardiac adverse effects Anorexia, nausea and vomiting Fatigue Visual disturbances ``` Drug Interactions: There are multiple drug interactions (p. 527, Burcham) Thiazides, loops - potassium Beta blockers, verapamil, diltiazem – decrease contractility Aminoglycosides, erythromycin, antacids – increase levels Captopril, alprazolam, amiodarone, diltiazem – increase digoxin by decreasing excretion Caution when patient is on multiple medications watch for signs of toxicity or subtherapeutic values ``` Routes po, SLOW IV Apical rate prior to administration Hold for <60 beats/minute Hold for change in rhythm Compliance is essential! ```
53
Aldosterone Antagonists for heart failure
- Spironolactone (Aldactone) - Eplerenone (Inspra) Mechanism of Action: Block aldosterone receptors in the heart and on bld vessels Drugs reduce the effects of aldosterone – which go beyond Na and water retention ``` Harmful effects of aldosterone no the heart : Promotes myocardial remodeling Promotes myocardial fibrosis Activate SNS Promotes vascular fibrosis Promotes baroreceptor dysfunction ```
54
Nitroglycerine for Heart Failure
Nitroglycerine Used in acute care Venodilator Decreases pulmonary congestion Adverse Effects: Hypotension and resultant reflex tachycardia
55
Device Therapy for Heart Failure
Implantable cardioverter defibrillator Cardiac resynchronization therapy Exercise training
56
Patient Teaching Points for Drugs and Heart Failure
Teach patients signs of toxicity Teach patients to monitor for rate and rhythm Teach patients to monitor for signs of hypokalemia
57
Drugs Affecting Lipids!!!!
Physiology Review: Classes of lipoproteins: -Six major classes of plasma lipoproteins -Three relevant to coronary atherosclerosis 1.Very-low-density lipoproteins (VLDLs) -AKA Triglycerides 2.Low-density lipoproteins (LDLs) -Cholesterol primary core lipid -Greatest contributor to . coronary heart disease (CHD) 3. .High-density lipoproteins (HDLs) Cholesterol as primary core lipid
58
Atherosclerotic Cardiovascular Disease (ASCVD)
-More than just deposit of lipids -Now considered primarily a chronic inflammatory process Infiltration of macrophages, T lymphocytes, and other inflammatory mediators In late stages of the disease inflammation weakens the atherosclerotic plaque leading to plaque rupture and then thrombosis SCreening and Risk Patients are screened for risk of developing ASCVD and considered for -statin treatment if they fall into one of the four different categories Cholesterol screening Every 5 years for adults older than 20 years
59
Factors in Risk Assessment
- Identifying CHD risk factors - Calculating 10-year CHD risk - Identifying CHD risk equivalents - Diabetes - Atherosclerotic disease other than CHD - Framingham risk score greater than 20% - dentifying an individual’s CHD risk category - Each type of dyslipidemia a patient has contributes independently to CHD risk
60
Therapeutic Lifestyle Changes
- Diet - Reduce intake of cholesterol and saturated fats - Minimize trans fat - Exercise 30-60 minutes on most days - Weight control - Smoking cessation
61
Classes of Antihyperlipidemics
Statins Fibric Acid Derivatives Nicotinic Acid Bile Acid Sequestrants
62
STATINS
``` Prototype: lovastatin (Mevacor) Highly effective and the most prescribed class of antilipids ``` Increase high-density lipoproteins (HDL) Decrease low-density lipoproteins (LDL), total cholesterol, very low-density lipoproteins (VLDL), and plasma triglycerides Competively inhibit HMG-CoA reductase Pregnancy category: X ``` Atorvastatin (Lipitor) Rosuvastatin (Crestor) Simvastatin (Zocor) Fluvastatin (Lescol) Pravastatin (Pravachol) ```
63
Lovastatin
Adverse effects: Elevated liver enzymes may occur with lovastatin and all other antilipid drugs. -Monitoring LFTs is essential. -Myopathy – injury to muscle tissue may occur. -Monitor CK (creatinine kinase) at baseline, repeat if symptoms (muscle aches, weakness) occur Metabolized via the hepatic enzyme CYP3A4: All drugs and substances (such as grapefruit juice) that inhibit this pathway may decrease metabolism and increase serum drug concentration.
64
Fibric Acid Derivatives
Lower triglyceride levels and increase HDL cholesterol Unlike the statins, effect on LDL cholesterol can be either to lower it slightly or to increase it slightly Gemfibrozil (Lopid) Clofibrate (Atromid-S)
65
Nicotinic Acid
Niacin -Reduces triglycerides -Reduces LDL cholesterol I-ncreases HDL cholesterol ``` Adverse effects: GI Upset Facial flushing Intense flushing of face neck and ears occurs in most patients Usually subsides several weeks ``` Can reduce by administering ASA 325 mg prior to taking Niacin
66
Bile Acid Sequestrants
Second- or third-line therapy Bind with the bile acids in the intestine to make them non-reabsorbable then excrete them: The lowered bile acid level prompts cholesterol to be used to make more bile acid. Cholestyramine (Questran) Colestipol (Colestid) Risk of hyperchloremic acidosis. Poor palatability, many GI adverse effects
67
Types of Angina
Stable Angina- predictable- usually upon exertion Unstable Angina- unpredictable chest pain Prinzmetal’s (variant ) Angina - happens when a pt is at rest, typically between midnight and 5 am
68
Nitrates
Prototype agent: nitroglycerin MOA: Relaxes vascular smooth muscle -Dilates both arterial and venous vessels: Venous dilation decreases peripheral resistance, thus decreasing BP. -Arteriolar dilation reduces systemic vascular resistance and arterial pressure, thus reducing afterload. -Decreases myocardial oxygen consumption -Redistributes blood flow in the heart, improving circulation to ischemic areas Tolerance to the vascular and antianginal effects may develop. Minimize by: Starting with as small a dose as possible Removing the NTG (paste or transdermal patches) from the patient for 8-10 hours usually at night
69
How to Give Nitrates
Acute angina: -Sublingual (SL) -Transmucosal T-ranslingual spray ``` Chronic recurrent angina: -Topical - NTG paste -Transdermal – NTG patch -Translingual spray T-ransmucosal or oral sustained-release - ``` Significant hypertension: Administer IV
70
Nursing responsibilities for Angina
Assess the patient’s BP and pulse prior to administration of nitrates. Acute care: IV access established Have the patient sit or lie down before taking NTG for acute pain. Repeat SL NTG every 5 minutes for up to three doses; assume myocardial infarction (MI) if no pain relief. Monitor for hypotension and reflex tachycardia. Common adverse effect: Headache.
71
How to store Nitrates
Loses potency with exposure to: - Light - Humidity - Heat - Plastic IV bags of fluid Sublingual NTG requires replacement every 3 months
72
Types of Nitrates
Nitroglycerine: - Isosorbide Mononitrate (Imdur, Monoket) . Sustained and immediate release - Isosorbide Dinitrate (Isordil) . Sustained and immediate release
73
Beta receptor antagonists and angina
Prevent stimulation of the beta receptors of the heart Slow the heart rate, depress atrioventricular (AV) conduction, decrease CO, and reduce BP, resulting in decreased oxygen demand Metoprolol Propranolol
74
Calcium CHannel antagonists and angina
Inhibit calcium from moving across cell membranes Slow the heart rate, depress impulse formation (automaticity), and slow the velocity of conduction, resulting in decreased oxygen demands of the heart Diltiazem (Cardizem) Verapamil Used in chronic stable angina when the patient cannot tolerate beta blockers or nitrates, or if the symptoms are not adequately controlled while on these therapies Drug of choice for Variant (Prinzmetal’s) angina
75
Adjunct Drug therapy and Angina
Acronym: MONA These therapies do not decrease oxygen demands on the heart, but slow down the progression of coronary artery disease or prevent/treat complications that may arise with angina.