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201 Cards in this Set
- Front
- Back
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What is Hypertension?
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-Systolic blood pressure of 140mm Hg or
-higher or a diastolic blood pressure of 90mm Hg or higher |
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Describe Primary Hypertension
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Characterizes 90% of hypertensive patients
-For these patients the cause is unknown |
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What type of killer is hypertension described as?
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The Silent Killer
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What is Secondary Hypertension?
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10% of HTN patients
-For these pts the cause is KNOWN. |
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What is the equation for BP?
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BP= cardiac output (CO) x peripheral vascular resistance (PVR)
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What is Cardiac Output?
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Stroke Volume x Heart Rate
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What 2 systems control blood pressure?
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-Sympathetic NS
-Renin-angiotensin-aldosterone system (RAAS) |
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What effect does the sympathetic NS have on BP?
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It works in the short term
-Ex: Regulation of BP laying down to standing up |
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How does RAAS effect BP?
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-Long Term effect
-Helps control of Na+/H2O levels. |
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What do HTN patients lack that non-HTN patients have?
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An Na+/H2O concetration set point and regulatory system
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Which receptor(s) does the Sympathetic NS act on to effect BP?
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-Activate B1: which increase HR and thus increase BP
-Activate A1 receptors which cause vasoconstriction and thus increase BP |
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What does Angiotensin II act as and which tissues does if effect?
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-It is a potent vasoconstrictor
-Acts on the blood vessels to cause vasoconstriction -Acts on the adrenal Cortex to enable Aldosterone to Increase Na+ and Water retention. |
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What enzyme converts angiotensinogen to angiotensin I?
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RENIN
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What is the purpose of ACE?
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To convert Angiotensin I to Angiotensin II
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Name the causes of increased Cardiac Output?
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-Increased fluid volume (excess sodium and water)
-Excess stimulation of RAAS -Sympathetic nervous system overactivity |
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How is the PVR increased?
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-Excess stimulation of RAAS
-Sympathetic Nervous System |
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What does water follow?
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Sodium
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How does the body react to diuretics?
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-Increases Urine Volume
-Decrease blood pressure |
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What does it mean to increase urine volume?
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Remove sodium and water from the body
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What is a long term effect of diuretics?
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Decreases PVR --> decrease in sodium content of smooth muscle cells
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Name the 2 examples of B-Blockers
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-Labetalol (Trandate)
-Metoprolol (Lopressor, Toprol XL) |
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What is the mechanism of action for B-Blockers?
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-Block B1 receptors in cardiac muscle
-Inhibits the release of Renin from the kidneys |
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When B1 receptors are blocked, what effects do we see on CO and HR?
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-Decrease in Heart Rate (negative chronotropic effects)
-Decrease in Cardiac Output (negative inotropic effects |
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What actions do only some B-Blockers have on BP?
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-Some agents inhibit activity of the sympathetic nervous system
-Some agents DIRECTLY decrease peripheral vascular resistance |
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What effects to B-Blockers have on blood volume?
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None!
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Which type of B-Blockers are contraindicated for asthma patients? Why?
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Non-selective B-Blockers because they can attache to B2 receptors in the lungs and cause bronchio constriction
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What is important to keep in mind with selective B-Blockers?
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Their selectivity is not absolute.
-Once you increase the dose, selectivity becomes non-selective |
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Describe the Intrinsic Sympathomimetic activity (ISA) of B-Blockers.
Is this good or bad? |
-Causes activation of adrenergic receptors producing effects similar to stimulation of the SNS
-Bad effect |
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What aspect of B-Blockers allow them to be widely distributed throughout the body?
What occurs during the hepatic metabolism of these B-Blockers? |
-Their lipid solubility
-The Lipid soluble agents undergo more extensive first pass hepatic metabolism |
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Does Lebatolol have Beta Selectivity?
Alpha blockade? ISA Activity? What degree is it's lipid solubility? |
-NO selectivity
-Yes alpha blockade -No ISA activity -Moderate Lipid solubility |
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What type of B-Blocker is Metoprolol?
Does it have alpha Blockade? Does it have ISA activity? What is its lipid solubiltiy? |
-B1 selective B-Blocker
-No alpha blockade -No ISA activity -Moderate lipid solubility |
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What cautions should be taken when taking pts off B-Blockers?
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-Must taper off over several weeks to avoid rebound hypertension
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Why should you keep watch of diabetics on B-blockers?
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-Keep watch of poorly controlled diabetic patients because they can MASK the signs and symptoms of HYPOGLYCEMIA!
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What are the adverse effects of B-Blockers?
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-Blocking B2 leads to bronchoconstriction
-Bradycardia -Weight Gain -CNS: sleep disturbances, depression, confusion, agitation, psychosis -Hypotension |
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How should a pt on B-Blockers get out of bed?
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They should sit for a period of time before getting up.
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List the most common Angiotensin-Converting Enzyme Inhibitors (ACEI)
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-Captopril (Capoten)
-Enalapril (Vasotec) -Lisinopril (Prinivil, Zestril) |
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What is the MOA of ACEIs?
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-Inhibit RAAS by preventing conversion of I --> II. Inhibit ACE
-Inhibiting II --> decreased PVR -->decreased blood pressure |
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What effect to do ACEIs have on bradykinin and prostaglandins? What does this do?
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-Limits the degradation of bradykinin (increases vasodilation)
-Increases synthesis of vasodilating prostaglandins |
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What is the PRIMARY effect of ACEIs?
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Decreases Peripheral Vascular Resistance
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What type of administration is used for ACEIs?
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All are oral except for enalaprilat which is IV.
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What is the best way to start a patient on an ACEI?
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Start them on a short acting agent (Captopril) and then switch to a longer acting once they are adjusted.
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WHat are the adverse effects of ACEIs?
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-Hyperkalemia--> arrhythmias
-Acute renal failure -angioedema -Cough |
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Which adverse effect of ACEIs is considered a true allergy?
When can it occur? What should you do? |
-Angioedema
It can occur at any point while patient is taking medication. --If it occurs you must seek immediate medical attention and stop all medications that can can cause angioedemas |
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Which adverse effect of ACEIs is not a true allergy?
What is it caused by? |
Cough
-Caused by an increase in bradykinin=irritant to the lungs = dry coughing |
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What drug interactions occur with ACEIs?
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Potassium supplements or potassium sparing drugs.
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As a nurse, what should you monitor for with pts on ACEIs?
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-any situations that might lead to a drop in fluid volume (V/D, dehydration, diaphoresis)
-Administer on an empty stomach 1 hour before or 2 hours after meals |
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What is the most popular drug under Angiotensin Receptor blocking agents (ARBs)
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Losartan (Cozaar)
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Which patients are prescribed ARBs?
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Ones that are intolerant to ACEIs
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What the MOA of ARBs?
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Selectively blocks the vasoconstrictive effects of angtiotensin II by blocking binding of II to its receptor
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What are the adverse effects of ARBs?
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-hyperkalemia
-Acute Renal Failure -Angioedema |
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What side affect do ACEIs have that ARBs do not?
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cough
-ARBs do no have an effect on Bradykinin |
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What are some common drug interactions for ARBs?
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-Potassium supplements
-Potassium sparing diuretics |
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Does a pt on ARBs have to consider mealtimes when administering the drug?
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No, unlike pts on ACEIs
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Give an example of a Direct Renin Inhibitor
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Aliskiren (Tekturna)
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Describe the MOA of Direct Renin Inhibitors
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-Bind to the active site of renin, preventing the cleavage of angiotensinogen and the formation of angiotensin I
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What ultimate effect do DRIs have on the body?
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They ultimately drop angiotensin II
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What are the adverse effects of DRIs?
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ANGIOEDEMA
-No cough! |
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Which drug cause angioedema?
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-ACEIs
-ARBs -DRIs |
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What is the only effect that ACEIs/ARBs/DRIs have on blood pressure?
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They only reduce PVR!
Have no effect on CO or Blood Volume! |
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What two classes of drugs fall under Calcium Channel Blockers?
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-Dihydropyridines (DHP)
Non-Dihydropyridines (non-DHP) |
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What is the most common DHP?
What is the most common non-DHP? |
DHP = Amlodipine (Norvasc)
non-DHP = Diltiazem (Cardizem) |
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What function do non-DHPs have that DHPs do not?
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They lower HR --> lowers CO --> lowers BP
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What is the MOA of CCBs?
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Calcium Channel Blockers
-Decreases PVR by blocking CALCIUM entry into smooth muscle --> vasodilation |
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Which CCB has a greater overall effect on BP?
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DHP lower BP much more than non-DHPs
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Which CCB has a greater effect on HR?
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non-DHP can lower HR, DHPs do not
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What effect do DHPs have on HR?
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They can actually increase HR causing REFLEX TACHYCARDIA
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-What are the adverse effects of Alodipine
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-DHP
-Reflex tachycardia -Headache and flushing -Peripheral edema |
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Bradycardia and Cardiac arrest are adverse effects of what drug?
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Diltiazem (Caedizem)
which is a non-DHP CCB |
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What are the Direct Vasodilator agents?
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-Hydralazine (Apresoline)
-Minoxidil (Loniten) Rogaine! |
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What MOA is used by Direct Vasodilators?
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-Causes artery relaxation (vasodilation) resulting in decreased blood pressure
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What can occur is Direct Vasodilators are administered alone?
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They can cause reflex tachycardia
∴They are usually combined with another drug |
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What are the adverse effects of Direct Vasodilators? When do these affects usually take place?
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-Tachycardia
-Fluid Retention -Usually occur early in administration |
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What effects do Direct Vasodilators have on PVR?
On CO? On Blood Volume? |
PVR= ↓
CO = ↑ Blood Volume = ↑ |
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What is Angina?
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Pain caused by body's response to lack of O2 in the heart
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What is stable angina?
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Pt experiences the same severity and frequency
-the characteristics of the pain are the same each out spurt |
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Describe unstable angina
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Frequency and severity of the pain increases over time
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What is Printzmetal?
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Variant angina:
Vasospasms occur at night |
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What medications are used to treat angina?
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-Nitrates
-Calcium Channel Blockers -B-Blockers |
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What is the mechanism of action for Nitrates?
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-Release nitric oxide (NO) --> Vasodilation
Preferentially relax VENOUS smooth muscle |
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Which smooth muscle do nitrates have a preference for?
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Venous! They Dilate it!
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What are the dosage forms for Nitrates?
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-IV
-Sublingual -Topical -Transdermal -Oral |
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Which dosage form of nitrates has the fastest onset of action?
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IV, followed by sublingual and then topical
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What are the DISADVANTAGES of Nitrates?
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-They can cause tolerance
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How do you prevent nitrate intolerance?
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You maintain a nitrate free interval:
-Don't use patches for 24 hours continuously -Don't use oral tabs (sustained release products) round the clock |
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What adverse effects are associated with nitrates?
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-Hypotension: Goes away over time
-Headache: due to the vasodilation |
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What are the common drug interactions with Nitrates?
What reaction do they cause? |
Erectile dysfunction drugs
-phosphodiesterase -5 inhibitors Viagra -Causes a cardiovascular event |
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How many total doses can a pt taking sublingual nitrates use until they have to go to the ER?
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Three
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How should a pt taking nitrates come off of the drug?
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They should taper of 4-6 weeks
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What are the treatment options to manage Chronic Heart Failure?
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-Manage fluid overload with diuretics
-Neurohormonal blockade with ACEI and B-Blockers -Digoxin |
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Where does Digoxin come from?
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Plant digitalis
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What is the MOA of digoxin?
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-Na+/K+ ATPase INHIBITOR --> enhances Ca++ entry into the cell--> increases contractility (positive inotropic)
-Slows the HR (negative inotropic) |
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What secondary therapeutic use does digoxin have other than the treatment of heart failure?
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It can treat atrial arrhythmias because it slows down HR
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Why is the half life of Digoxin dependent of renal function?
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Because it is renally eliminated and NOT DIALYZABLE!!
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What is important to remember about the dosage forms of digoxin?
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They are no interchangeable between mg to mg
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What are the early signs of toxicity for Digoxin?
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-N/V/D and abdominal pain!
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What symptoms are experienced by patients that are TOXIC with DIGOXIN?
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Headache, visual disturbances (green/yellow halos)
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What is a common adverse effect of digoxin that does not indicate toxicity?
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Cardiac arrhythmias
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Which digoxin patients must you take strict caution with?
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Those that have impaired renal function
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What should digoxin patients avoid eating when taking their meds>?
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Good or antacids
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In general, what is cholesterol?
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-Soft, waxy substance found among the lipids in the blood stream
-Used to form cell membranes and some hormones |
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What do high levels of cholesterol make a person susceptible to?
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Coronary Artery Disease
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What is LDL-Cholesterol?
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Low-density lipoprotein
-Bad cholesterol |
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What do High levels of LDL-cholesterol do in the blood?
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They cause slow build up of plaques in the walls of arteries
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What is HDL-Cholesterol?
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High-Density Lipoprotein
-Good Cholesterol -Carries cholesterol away from arteries and back to liver |
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What can high levels of HDL protect against?
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Heart Attack
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What are the drug therapy options for the treatment of hyperlipidemia?
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-Bile Acid Sequesterants
-Niacin -Fabric acid derivatives/ Fibrates -HMG-CoA reducate inhibitors -Cholesterol absorption inhibitors -Fish oils |
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What are the Bile Acid Sequesterant agents?
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-Cholestyramine (Questran)
-Coletipol (Colestid) |
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What is the MOA of Cholestyramine and Coletipol?
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-Bile Acid Sequestrants
-Bind bile acids which are precursors to cholesterol (in the GI tract) preventing their absorption |
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What are Bile Acid Sequesterants used for?
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To LDL reduction
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What adverse reactions are associated with Cholestyramine and Coletipol?
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Bile Acid Sequesterants
GI effects: -Constipation, diarrhea, nausea, flatulence. |
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What are the drug interactions for bile acid sequesterants?
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Cholestyramine and Coletipol bind to many drugs in the gut!
-So administer other drugs at least 1 hour before or 4-6 hours after |
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What patients are not recommended taking Bile Acid Sequesterants?
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Patients that are not compliant with medication regimes
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What is the MOA of of Niacin (Niaspan) (Nicotinic Acid)
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-Inhibits release of free fatty acids from adipose tissue
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What is Niacin used for?
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To reduce tryglyceride levels
-Moderate reduction of LDL -Moderate increase in HDL |
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What are the contraindications of NIACIN?!
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-Active/chronic liver disease
-Recent peptic ulcer (irritating to the GI tract) -Excessive alcohol use (liver damage) |
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What are the adverse effects of Niacin?
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-Flushing, N/V/D
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What should a pt on Niacin do to limit the adverse effects?
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-Take aspirin or ibuprofen 30 minutes before niacin to limit flushing
-Take niacin with food to help with GI upsets |
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What are the Fibric Acid Derivative (Fibrates) agents?
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-Gemfibrozil (Lopid)
-Fenofibrate (Tricor) |
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What is the MOA of Gemfibrozil and Fenofibrate?
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--Fibrates
-Elimiation of tryglyceride rich particles -Moderate decrease of LDL -Moderate increase in HDL |
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What are the contraindication for Fibrates?
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Severe hepatic and renal dysfunction because they are metabolized in the liver and excreted in the kidneys
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The adverse effects of N/V abdominal pain and MUSCLE WEAKNESS are related to which drugs?
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-Fibrates
-Gemfibrozil -Fenofibrate |
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What are the most commonly prescribed class of drugs to treat high cholesterol?
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HMG CoA-Reductase Inhibitors
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What are the HMG CoA-Reductase inhibitor agents?
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-Atorvastatin (Lipitor)
-Pravastatin (Pravachol) -Simvastatin (Zocor) |
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What MOA is used by HMG-CoA Reductase inhibitors>?
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Inhibits HMG-CoA reductase enzyme, which is involved in the production of cholesterol
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What are the most effect agents for LDL reduction?
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HMG-CoA Reduc Inhibitors
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What overall effects do the "statins" have on cholesterol levels?
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-HMG-CoA Reduct Inhibitors
-They most effective in lowering LDL -moderate effect in raising HDL -Moderate decrease in tryglyceride concentrations |
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How are HMG-CoA's metabolized and excreted?
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-Most are hepatically metabolized
-Some are renally excreted |
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When should pts take their HMG-CoAs?
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at bedtime because that is when liver function is at its highest
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What property of HMG-CoAs causes them to have a lot of drug interactions?
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They are highly protein bound
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Which class of drugs is under a pregnancy category X?
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HMG-CoA reductase Inhibitors!!!
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What are the contraindications for the "statins"?
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HMG-CoAs
-Chronic/active liver disease -Persistent increase in liver function tests -Use with caution with excess alcohol consumption |
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What are the adverse effects for the Statins?
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HMG-CoAs?
-Transient GI complaints -Muscle weakness, break down of muscle (rhabdomyolysis) (exasperated if taken with fibrates) |
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What are the Drug interactions for HMG-CoAs?
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-Inhibitors of CYP 450
-DISPLACEMENT (resulting in more free/active drug) -Grapefruit juice: risk of toxicity |
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What drug falls under Cholesterol Absorption Inhibitors?
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-Ezetimibe (Zetia)
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What is the MOA of Ezetimibe?
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-Cholesterol Absorption inhibitors
Inhibits cholesterol absorption by the small intestine |
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What is Ezetimibe used for?
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Used to reduce LDL cholesterol
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What are the contraindications for Cholesterol Absorption Inhibitors?
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-Active Liver disease
-Persistant elevation of liver function tests |
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What adverse effects are associated with Ezetimibe?
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-Transient GI complaints
-Muscle Weakness |
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Are Fish Oils used as a primary intervention for cholesterol?
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No, they are a secondary
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Why are fish oils used to treat hyperlipidemia?
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Evidence suggests Omega-3-Fatty acids reduce risk of Coronary events in patients with CHD
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What is the major side effect for Fish Oils?
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Diarrhea
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What is the primary action of platelets?
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Aggregation onto damaged tissue to them form a clot?
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What is the function of Fibrin?
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Fibrin acts to hold the blood clot, formed from the aggregation of platelets, together.
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What are the Anitplatelet Agents?
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-Cyclooxygenase inhibitors
-Adenosine diphosphate (ADP) inhibitors -Adenosine reuptake inhibitors -Glycoprotein IIb/IIIa inhibitors |
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What is the main Cyclooxygenase Inhibitor?
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Aspirin
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What is the MOA of aspirin?
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IRREVERSIBLE inhibition of platelet cyclooxygenase-1
-Blocks the formation of thromboxane A2 (potent stimulator of platelets) from arachadonic acid |
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What happens to the platelet once aspirin has worked on it?
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The platelet is essentially dead
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How often do platelets regenerate?
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About every 7 days
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What is the half life of aspirin?
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15 - 20 mins
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How long do the effects of aspirin last?
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The life span of the platelet
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Where is aspirin absorbed?
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Rapidly absorbed in the stomach and upper intestine
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What is the predominant adverse effect of Aspirin?
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Bleeding
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What are the Adenosine Diphosphate (ADP) inhibitor agents?
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-Ticlopidine (Ticlid)
-Clopidogrel (Plavix) -Prasugrel (Effient) |
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What is the MOA of Ticlopidine, Clopidogrel and Prasugrel?
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-ADP inhibitors
-IRREVERSIBLY inhibit ADP pathway receptor to inhibit platelet aggregation |
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What effects do ADPIs have on thromboxane A2 or prostacyclin synthesis?
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None
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What drug acts synergistically with aspirin?
|
ADP Inhibitors
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What type of drug are ADP inhibitors considered?
|
PRODRUGS
-must be metabolized by the liver to active metabolite |
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How long doe the effects of ADP inhibitors last?
|
The lifespan of the platelet
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What are the adverse effects of Ticlopidine, Clopridogrel and Prasugrel?
|
ADP Inhibitors
Bleeding --> greater if given with aspirin |
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What drug is an Adenosine Reuptake Inhibitor?
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-Dipyridamole (Persantine)
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What is the MOA of Dipyridamole?
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-Adenosine Reuptake Inhibitor
-vasodilator that inhibits platelet function by inhibiting adenosine uptake? |
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Why is Dipyridamole usually administered along with another drug?
|
Because it has little to no beneficial effect by itself
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What is Aggrenox?
|
Drug combination of Aspirin and the Adenosine Reuptake Inhibitor Dipyridamole
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What are the adverse effects of Dipyridamole?
|
Adenosine Reuptake Inhibitor
-Bleeding usually not associate with dipyridamole alone |
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What are the agents of Glycoprotein IIb/IIIa Inhibitors?
|
-Abciximab (ReoPro)
-Tirofiban (Aggrastat) -Eptifibatide (Integrilin) |
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What is the MOA of Abciximab, Tirofiban and Eptifibatide?
|
Glycoprotein IIb/IIIa Inhibitors
Inhibit formation of platelet thrombi by inhibiting activated receptors from binding with fibrinogen and forming bridges between activated platelets |
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What are the adverse effects of Glycoprotein IIb/IIIa Inhibitors?
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-Thrombocytopenia (low platelet count)
-Bleeding |
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During coagulation, two pathways come together at which factor?
|
Factor X
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What are the Anticoagulant Agents?
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-Unfractionated Heparin
-Low molecular weight heparins -Factor Xa inhibitors -Direct thrombin inhibitors -Warfarin (Coumadin) |
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What is the MOA for unfractionated Heparin?
|
-Binds to antithrombin III (normal anticoagulant in the body) --> enhaces its activity
-ATIII binds to factors IIa, IXa, Xa, XIa and XIIa --> inhibits their activity |
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What effect does unfractionated heparin have on formed thrombi?
|
NONE, formed clots must be removed by physiologic thrombolytic mechanisms
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Why must heparin pts have their blood taken often?
|
Because of Heparin's unpredictable activity
-only 1/3 of heparin molecules have anticoagulant activity |
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What is the composition of unfractionated heparin?
|
Heterogenous mix of complex mucopolysaccharide
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Why can't unfractionated heparin be administered via IM?
|
Can cause an acute Hematoma
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How should unfractionated Heparin be administered?
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Sub Q or IV
-Oral is poorly absorbed |
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What is the elimination and dosing of unfractionated Heparin?
|
Elimination: Metabolized by hepatic heparinases (enzymes)
Dose: based on weight |
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What are the adverse effects of Unfractionated Heparin?
|
-Bleeding
-Thrombocytopenia -Osteoporosis |
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How should you treat an overdose of unfractionated Heparin?
|
Give the REVERSAL AGENT: PROTAMINE
- |
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What is Protamine?
When is it used? How does it work? |
Reversal agent for unfractionated Heparin
-Combines ionically with heparin -For treatment of a heparin overdose |
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What is the disadvantage of using Protamine?
|
Heparin reversal agent
-It can cause anaphylaxis in allergic patients |
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What are the agents of Low Molecular Weight Heparin?
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-Enoxaparin (Lovenox)
-Dalteparin (Fragmin) Tinzaparin (Innohep) |
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What is the MOA of Enoxaparin, Dalteparin and Tinzaparin?
How are they administered/ |
Low Molecular Weight Heparins
-Inhibit factor Xa > factor lia -Administer Sub Q |
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Why are low Molecular Weight Heparin preferred over Unfractionated Heparin?
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They have a more predicatable anticoagulant effect
-They don't need as much monitoring |
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What is the onset of action for LMW Heparin and how is it eliminated?
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Onset 3-5 hours after Sub Q
-Eliminated via Kidneys |
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What are the adverse effects of LMW Heparin?
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-Bleeding
-Thrombocytopenia -Injection site reactions -Osteoporosis |
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What is the Factor Xa Inhibitor agent?
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-Fondaparinux (Arixtra)
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What are Factor Xa Inhibitors made of?
How are they administered? Adverse effects? |
-Synthetic polysaccharides
-Sub Q admin -same adverse effects as LMW heparin Caution with renal failure patients |
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What is the MOA of Thrombin Inhibitors?
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-Block either active site or both active site and exocite I
-Binds to thrombin: INHIBITS FREE AND CLOT-BOUND THROMBIN without requiring endogenous cofactors |
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What are the direct thrombin inhibitor agents?
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-Lepirudin (Refludan)
-Bivalirudin (Angiomax) -Argatroban (Novastan) |
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How are direct thrombin inhibitors administered?
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All via IV
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What are the adverse effects of Lepirudin, Bivalrudin, Argatroban?
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Direct Thrombin Inhibitors
-Bleeding |
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What is the MOA of Warfarin?
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Inhibits the synthesis of Vitamin K dependent clotting factors
(Factors II, VII, IX and X) |
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What is the overall outcome of Warfarin?
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Doesn't dissolve current clots
-Prevents growth and helps to shrink over period of time |
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How much of Warfarin is absorbed?
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100%
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Why does Warfarin have many D/D interactions?
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Because it is 99% protein bound
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What if your patient needs to be on coumadin and Heparin?
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There is a 5 day overlap
-Heparin acts immediately (acute situation) -Coumadin kicks in after 5 days Then the pt can come off of heparin and just be on coumadin |
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What do you monitor for Coumadin pts?
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-International Normalized Ratio (INR): goal is determined by indication
-Monitor for signs of bleeding |
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How is Warfarin Metabolized?
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Hepatically CYP 3A4 and CYP 2C9
-Metabolism rate differs from person to person |
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What are the drug interactions for Warfarin?
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-CYP inhibitors will increase warfarin concentrations
--Recommend: reduce warfarin --Ex: amiodarone, voriconazole, fluconazole CYP inducers will decrease warfarin concentrations --Recommend: increase warfarin dose --Ex. carbamazapine, phenytoin, rifampin |
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What are the adverse effects of Warfarin?
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-Bruising
-Bleeding -Teratogenic: PREGNANCY X |
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How do you reverse the effects of Warfarin?
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with VITAMIN K
-Promotes hepatic formation of factors required for normal clotting -Admin: orally, subQ or IV |
