Week 4 - Pharmacology

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Week 4 - Pharmacology
2013-07-21 23:00:36
Antihypertensives Antidysrhythmics Antianginals Glycosides Shock

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  1. ***Diuretics***
    • Drugs that block reabsorption of Na from the tubules produce the greatest amt of water loss (water follows salt) 
    • -proximal & loop drugs more powerful than distal drugs in reducing fluid 
    • -Must drink water with these pills!
  2. Proximal Tubule Diuretics
    • Prototype: Acetazolamide (Diamox)
    • Inhibits carbonic anhydrase, preventing reabsorption of bicarbonate ions, resulting in increased osmotic diuresis (urine production)
    • Used for mtn climbers for altitude sickness (won't see much for HTN)
    • Contraindications: allergy to sulfonamides
    • Drug-Drug interactions: amphetamines
    • *Older adults susceptible to excessive water loss (hypotension), diabetics will have a higher blood sugar levels, and kidney stones possible
  3. Mannitol
    • Osmotic diuretic, potent osmotic
    • Stays in tubule
    • its large size pulls water and solutes into the tubular fluid, and less Na, Cl, and water are reabsorbed
    • Crystallization is common, so nurse must warm up (warm water bath)
    • Indwelling catheter w/ urometer to measure hourly urine output
  4. ***Furosemide (Lasix)***
    • Indications: significant edema, HTN
    • Inhibits reabsorption of Na and Cl in the ascending loop of Henle
    • Similar to thiazides but more intense
    • Fairly well absorbed, peak 1-2 hr, IV affect w/in 5 mins
    • OD: hypotension, hypovolemia, electrolyte imbalances
    • Education: Postural (orthostatic) hypotension, foods rich in K, K supplements, avoid sun, alert to hearing loss
  5. ***Hydrochlorothiazide (HCTZ)***
    • Thiazide
    • Indications: Essential HTN, chronic edema, hypercalciuria and stone formation
    • Inhibits Na and Cl reabsorption in early distal tubule
    • Reduces plasma and extracellular fluid
    • Has direct action on peripheral vessels to decrease peripheral resistance 
    • Inhibits release of insulin, raises sugar
    • SE: hyponatremia, hypovolemia, polyuria, hypokalemia, increased risk of digitalis toxicity
    • Contraindications: Renal disease, Gout, pregnant women
    • Ed: Supplement K in diet, Need monitoring of BP & lipid levels, Drug may make lethargic
    • *Best time to take med is breakfast* (so not peeing all night)
  6. Spironolactone (Aldactone)
    • Potassium-sparing Diuretic
    • Block axn of Aldosterone (which retains Na) in the distal tubule, promotes Na and water excretion 
    • allows K to remain in the system
    • *Must monitor K to make sure levels don't get too high*
    • Indications: prevention & treatment of hypokalemia, HTN, edema
    • Increases 1/2-life of Dig
    • decreases effects of anticoagulants
    • Chemically like steroid hormone: likely to see gynecomastia (growing boobs), menstrual irregularities, impotence, hirsuitism (growing hair)
    • Ed: unlike other diuretics, don't push K+ foods
  7. ***Nursing Issues in Diuretic Therapy***
    • Compliance:
    • -An obvious increase in urine may only last a few weeks, but drug is still needed -> pt may stop or self-increase dose
    • -Avoiding inopportune times: tailor med schedule to lifestyle
    • Diet: Low/controlled salt intake, must take in adequate water! 
    • Signs of Hypovolemia: dizziness, confusion, insatiable thirst, salt craving
    • Signs of Hypokalemia: thirst, muscle weakness, lethargy, depression, muscle cramping, vomiting
    • Controlling K levels: K-sparing diuretics, IV K+ supplement
  8. ***Beta Blockers***
    • Beta1 - referred to as cardioselective b/c block receptors in the heart (increase HR, so beta blocker would decrease HR)
    • Beta2 - primarily in smooth muscle and lungs (bronchodilator, so beta blocker would constrict)
    • Decrease HR, conduction, contractility, and CO
    • Inhibits release of renin from kidney
    • decreases peripheral vascular resistance -> lowers BP
    • Action: bronchoconstriction, masks symptoms of hypoglycemia
    • Slows heart rate, conduction, & contraction
    • -Lower CO = drop in BP
    • Rebound HTN stroke possible if stop
  9. ***Propranolol (Beta blocker)***
    • indications: Chronic angina, cardiac dysrhythmias, prevents second MIs, treats vascular HA, tremors, anxiety
    • ActionDecreases cardiac contractility (neg inotropic affect), dropping arterial pressure and inhibits renin release (from kidney) 
    • Esp. useful in HTN w/ tachycardia, angina (chest pain)
    • *More likely to see atenolol or metropolol in clinical practice*
    • SE: Bradycardia, fatigue, drowsiness, depression, impotence, cold hands and feet, CHF
    • D-D interaction: MAOIs (antidepressant drugs), blocks sympathomimetics
    • Ed: Don't alter drug regimen, be consistent w/ or w/o food, No OTC decongestants, diet and weight management, If pulse <45 don't give, Monitor depression (b/c of lethargy, not causing depression)
  10. Rebound Hypertension
    • If pt suddenly stops the med treating HTN, then there could be a rebound b/c body tries to make up for low levels and overshoots, causing even higher BP and can lead to stroke. 
    • -Massive sympathetic "rescue" causes rapid HR and BP
  11. ***Verapamil***
    • Calcium-channel blocker
    • Indications: HTN, angina, prophylaxis for vascular headaches
    • Actions: decreases force of myocardial contraction by blocking inward flow of Ca into cells
    • -Decreases automaticity of SA node or conduction through AV node (negative dromotropic effect) 
    • -Coronary artery dilation, lowering coronary resistance and improves coronary blood flow
    • -Peripheral dilation which lowers peripheral resistance
    • SE: HA, GI sx, hypOtension, flushing/rash, edema, dry mouth, constipation
  12. ***CCB (Ca channel blockers) Cautions***
    • Patients with renal or hepatic dysfunction may have reduced clearance of drugs
    • Older adults more susceptible to SE
    • Education:
    • -If extended release, do not chew or crush
    • -Take HR before dose (must be at least 45)
    • -Can make HF worse
    • -Support hose/elevation of legs (a little edema)
  13. ***ACE inhibitors (Angiotensin-Converting Enzyme)***
    • Anti-HTN drug
    • Action: Completely blocks the Angiotensin I converting enzyme 
    • -prevents the production of Ang II, which is powerful vasoconstrictor
    • -decreases vascular tone
    • -Absence of aldosterone release leads to excretion of fluid
    • -Renal protective in diabetics
    • Works the best with least SE
    • Do not use when pregnant
  14. ***Captopril (Capoten)***
    • ACE inhibitor
    • Indications: Essential HTN w/ normal renal fxn
    • -often used w/ a thiazide or loop diuretic (Counteracts K retention of ACE)
    • -Diabetes: for renal protection even w/o HTN (small dose)
    • *This med works well w/ most people; easily combined with other drugs, remodels heart after MI, holds on to K+
    • SE: hyperkalemia, dry cough, angioedema (blisters) 
    • D-D interactions: additive effect w/ antihypertensives
    • Ed: Full effects not seen for weeks, taste impairment (goes away in 2-3 wks), cough is not a disease, do not use K supplements or pregnancy (CATEGORY X!!)
  15. ***Angiotensin II Receptor Blockers (ARBs)***
    • PrototypeLosartan (Cozaar) 
    • -Action: more specific than ACE; vasodilation via smooth muscle relaxation; doesn't retain K as much as ACE; DM protection like ACE
    • Decreased water volume and Na

    • Prototype: Aliskiren (Tekturna)
    • -Action: Binds w/ renin, inhibiting change from angiotensinogen to angiotensin I
    • -Indications: Essential HTN
    • -SE: cough, hyperkalemia, angioedema, diarrhea
  16. Sympatholytic Drugs
    • Synergistic effect with other antihypertensives
    • Reduces renal blood flow
    • orthostatic hypotension
    • may impair sexual fxn
    • psychiatric disturbances (nightmares)
    • Overdose: severe hypotension, CV collapse
  17. Clonidine (Catapres)
    • Central-acting Sympatholytic
    • Indications: Moderate HTN
    • Action: decreases sympathetic outflow from brain to periphery - lowers CO, HR, peripheral resistance
    • SE: General ones + risk for rebound HTN if drug abruptly withdrawn
    • D-D interaction: use with Beta blocker counteracts effects and can lead to severe HTN
    • OD: severe hypotension or severe hypertensive crisis
  18. ***Doxazosin (Cardura)***
    • Peripheral-acting Alpha Adrenergic Blocker
    • Indications: Step II drugs b/c of SE or in pts with hyperlipidemia
    • Action: Blocks alpha1 receptors, resulting in vasodilation and lowered peripheral vascular resistance
    • -Less cardiac effects b/c no beta action
    • -Can cause orthostatic hypotension in first dose or w/ dosage increases
    • -Relaxes urinary sphincter tone
    • SE: weakness, GI sx, stuffy nose, edema of lower extremities, HA, syncope, SOB
    • Ed: "first-dose hypotensive rxn" - warn to avoid rapid postural changes; effects may not be achieved until 4-6 wks, may relax bladder sphincter too much
  19. Direct-acting Vasodilator
    • Direct effect on smooth muscle walls of veins and arterioles, lowers peripheral resistance and BP
    • -Drop in BP stimulates baroreceptors -> increases BP and CO and release of renin
    • Prototypes: arteriolar dilators, arteriolar and venous dilators
  20. ***Amiodarone (Cordarone)***
    • Group III - Potassium channel blocker
    • Indications: Life-threatening ventricular dysrhythmias and atrial fib conversion
    • Action: Prolongs action potential, increases refractory period in all cardiac tissues
    • -decreases automaticity, prolongs AV conduction, blocks Na/K/Ca channels
    • SE: Complex and serious effects on lungs (creates fibers making lungs stiff and full of scar tissue so that O2 transport is poor)
    • -Bitter taste, tremors, numbness and tingling of fingers, blue-grey skin color, cough, dyspnea, blurred vision
    • D-D interactions: increases affect of dig, anticoagulants 
    • -Can cause life-threatening rhythms
  21. ***Hyperlipidemia***
    • Metabolic disorder: increased concentration of cholesterol and triglycerides
    • Atherosclerosis: Lipid deposits in linings of large and medium-sized arteries, eventually produces degenerative changes and obstructing blood flow; can rupture and block or become emboli
    • Key factor: when there is inflammation, cholesterol is more likely to be deposited
  22. ***Hyperlipidemia treatment options***
    • Initial: 
    • -Lifestyle modification for 3-6 months: reduce daily intake of fat, cholesterol, calories; reduce alcohol, smoking; exercise! whole grains, less refined sugars
    • -Reduce lipid elevating drugs: thiazides, some beta blockers, estrogens mixed w/ progestins
  23. ***Antilipemic Agents***
    • Reduce progression of atherosclerosis and improve morbidity in pts at risk (few have actually reduced size of plaques, but lipitor can!)
    • Main types: bile acid sequestrants, cholesterol synthesis inhibitors
  24. ***Statins***
    • Those mixed w/ anti-lipemics more likely to have issues
    • Stronger the statin, the more risks (risks run in families)
  25. ***Lovastatin (Mevacor)***
    • Effect: most effective drugs to lower LDL
    • -inhibits critical enzyme in formation of cholesterol (HMG-CoA), thus ↓ total cholesterol, LDL, VLDL, and triglycerides while also increasing HDL
    • For primary hyperlipidemia that doesn't respond to diet alone
    • SE: (few) HA, GI sx, myalgia, liver dysfunction, 
    • D-D interactions: (few) cyclosporin (immunosuppressant) increases severe SE; grapefruit juice (increases free dose of other drugs) 
    • Toxicity: increased risk w/ taken with gemfibrozil or niacin
  26. ***Omega 3 Fatty Acids***
    • Fish or shrimp source
    • Must be taken 3x/day 
    • Fish burp 
    • Potential issues with shellfish allergy
    • Will raise LDL
    • Potential for heavy mercury toxicity
    • Rx form is Lovenza.
  27. ***Cardiac Glycosides***
    • Used for cardiac disease & HF
    • Extremely narrow therapeutic range
    • Toxicity is life-threatening
  28. ***Chronic Heart Failure (CHF)***
    • Body responses to CHF: ↑ HR, BP, myocardial workload, O2 demand; worsening of edema, weight gain, SOB, dyspnea, neck vein distension, hepatomegaly
    • Drug Therapy: (general aim is to benefit heart or kidneys) improve cardiac contractility (ACE inhibitors/ARBs, cardiac glycosides), reduce preload (diuretic to reduce excess fluid), reduce afterload (vasodilators), ventricular restructuring and rate control (beta-blocker)
  29. ***Digoxin (Lanoxin)***
    • Cardiac Glucoside
    • Indication: CHF, atrial fibrillation or other supraventricular dysrhythmia when ventricular rate is too rapid
    • Action: positive (speed up) inotrope, negative (slow down) chronotrope, neg dromotrope; potent, small doses
    • ADME: PO, IV, IM; t1/2 = 36 hrs (given once a day b/c hard to take every 36 hours); narrow therapeutic range: 0.5-0.8 mg/mL
    • Indirectly ↓ HR and ↑ Na and water excretion
    • *A loading dose is always used for people in really bad shape: dose depends on weight, rapidly done for acute problems, elderly prefer to do gradually
    • SE: cardiac (bradycardia, AV block), GI sx, vision (green/yellow tint to white objects and halos around lights), gynecomastia w/ long-term use
    • *Therapy monitoring is important; HR prior to dosing; must take apical pulse for 1 min and hold drug if <60 (take apical b/c there may be a pulse deficit, or a diff btw apical and radial pulse)
    • Toxicity: n/v, vision changes, dysrhythmias (treat by holding doses, then digibind or other subs to hasten elimination)
    • -Hypokalemia most common cause of dig overdose
    • -Hypomagnesemia increases risk of toxicity
    • -Hypercalcemia and hyperkalemia may cause dysrhythmias
    • D-D interactions: many! Ex) if take with OTC decongestants = dangerous!! 
    • Nursing considerations: 
    • -watch for HR or dysrhythmias
    • -Monitor electrolyte imbalances
    • -Check if other drugs change lytes
    • -Renal insufficiency pts are more easily toxic b/c of decreased excretion of dig.
    • -Death rate higher in females
  30. ***Dopamine***
    • Mainstay for ICU care for shock
    • Hung as a titratable drip
    • Pt is closely monitored to determine BP, CO, pulse and other vital parameters
    • Massive vasoconstrictor, so if gets into surrounding tissues, tissues will be infiltrated and die (tissue will slough) - barely see this med given anymore
    • Watch IVs like a hawk!