DRUGS AFFECTING THE CARDIOVASCULAR SYSTEM Flashcards by Angeline Plaza

The common and biggest problem in the
cardiovascular system is hypertension. All
hypertension is treated by antihypertensive
medications.

Drug used to treat high blood pressure or
hypertension

Giving of hypertensive medication seeks the
prevention of further complications related to this
cardiovascular disease

ANTIHYPERTENSIVES

How well did you know this?

Not at all

Perfectly

What do we particularly prevent if we have
hypertension?

Stroke and myocardial infarction

How well did you know this?

Not at all

Perfectly

○ ACE Inhibitors
○ Vasodilators
○ Angiotensin II receptor blocker
○ Calcium Channel Blocker
○ Sympatholytics

Antihypertensives

How well did you know this?

Not at all

Perfectly

Also called as water pills because they design to
increase the amount of water and salt that is expelled
out of our body in a form of urine; increase the
amount of water and sodium that is expelled out of
our body in the form of urine, so that there will be
normal or homeostasis on our fluid in the body.

They are usually/ often prescribed for the patients
who have high blood pressure/ hypertension. This is
also used not just for hypertension but different
illnesses including congestive heart failure as well as
the edema.

Used to reduce the amount of fluid in our blood
vessels so that there will be lower blood pressure to
our patients.

xxxxx for patients with Congestive Heart Failure
(CHF) is used for effective pumping of blood in the
body.

DIURETICS

How well did you know this?

Not at all

Perfectly

If BP is high, the heart compensates, this is
why the heart beats fast, contractions are fast.
Fluid overload occurs in the body which may
lead to cardiac tamponade.

For edema, patients may have the possibility of
atelectasis, fluid accumulation not only in
certain parts of the body but also in the pleural
cavity where the lungs may collapse. The heart
may also suffer from irregularities if there is
edema. Physiologic functions are also altered.

Diuretics notes

How well did you know this?

Not at all

Perfectly

○ Thiazide
○ Osmotic
○ Loop
○ Potassium-Sparing

Diuretics

How well did you know this?

Not at all

Perfectly

Used to provide immediate relief from symptoms that
might prevent anginal attacks. This is also the Drug of
Choice (DOC) for patients complaining of angina.

Anginal is the medical term for chest pain, also
known as angina or angina pectoris

ANTI- ANGINAL

How well did you know this?

Not at all

Perfectly

○ Nitrates
○ Non-nitrates

ANTI- ANGINAL

How well did you know this?

Not at all

Perfectly

is the problem of the heart that entails the
electrical system of the heart. This is when the heart
may be beating quickly or have irregular waves.

Arrhythmia

How well did you know this?

Not at all

Perfectly

defibrillator is used to bring shock to the heart

Flatline or asystole

How well did you know this?

Not at all

Perfectly

➢ Atrial Fibrillation
➢ Ventricular Fibrillation
➢ Atrial Flatters

IRREGULARITIES IN ECG TRACING

How well did you know this?

Not at all

Perfectly

These are arrhythmic disorders corrected by
anti-arrhythmic drugs. Not only medications but also atrial
shocks brought by defibrillation can also be used to address
the problem.

IRREGULARITIES IN ECG TRACING NOTE

How well did you know this?

Not at all

Perfectly

These are classification of medicines that are
commonly derived from herbal medicine or herbal
drugs
e.g. foxglove plant
The most common xxxxxxxxxx is digoxin. It is
used for patients that have atrial fibrillation and atrial
flatters.

CARDIAC GLYCOSIDES

How well did you know this?

Not at all

Perfectly

if this happens efficacy is better. Though, consider the status of the patient. If the pt. is not allergic to certain medications and if their kidneys are not damaged.

If a patient has a pre-existing problem, the metabolism and excretion of the drug is altered. This is why a patient’s history is important.

Cardiac Glycosides are also used for patients who
have CHF, if other medications are ineffective

DRUG INTERACTION: ANTI-ARRHYTHMIC + CARDIAC
GLYCOSIDES = DOUBLED EFFECT

How well did you know this?

Not at all

Perfectly

Anticoagulants
Thrombolytics

DRUG AFFECTING THE BLOOD

How well did you know this?

Not at all

Perfectly

(stop blood clotting; blood thinner)

➢ They are used to stop the blood from thickening
or clotting
➢ They simply interrupt the body’s natural clotting process, they alter clotting factors to prevent thrombosis

Anticoagulants

How well did you know this?

Not at all

Perfectly

= (thrombolysis? ; already has pre-existing clot)

they are used to dissolve clots

Thrombolytics

How well did you know this?

Not at all

Perfectly

How are thrombolytics different from anticoagulants?

Anticoagulants are blood thinners, natural clotting
factors are not that activated through them.
Thrombolytics on the other hand, with a pre-existing
clot, will dissolve it so that it will not flow together in
the bloodstream and cause blockage on veins and
arteries which can improve blood flow thus preventing
damage on the organs by not blocking the blood
supply of which may lead to the death of cellular walls
and tissues if it happens.

How well did you know this?

Not at all

Perfectly

➢ These are medications that are administered intravenously especially during emergencies.
➢ In the case of bleeding incidents, hemostatics are given to stop the bleeding and prevent hemorrhagic shock because of ruptured blood vessels

Hemostatics

How well did you know this?

Not at all

Perfectly

❖ Part of its anatomy is the superior and inferior vena cava where the blood flows from the system to the pulmonary and etc.
➔ Pulmonary veins
➔ Right Atrium
➔ Pulmonary Valve
➔ Tricuspid valve
➔ Right Ventricle
➔ Aorta
➔ Pulmonary Arteries and Veins (both left and right)
➔ Left atrium
➔ Mitral Valve
➔ Aortic Valve
➔ Left Ventricle
❖ The heart has right and left sides and both work as
separate pumps
❖ Blood Pressure: due to the pump or pressure that the
heart is giving out
❖ If the heart is divided into right and left pumps, it has 4
chambers
● Atrium (Right & Left) as the receiving
chambers
● Ventricles (Right & Left) as discharging
chambers

ANATOMY OF THE HEART

How well did you know this?

Not at all

Perfectly

Deoxygenated blood flows from system through the superior
and inferior vena cava → Right Atrium → Tricuspid Valve
→ Right Ventricle → Pulmonary Semilunar Valve →
Pulmonary trunk → Right & Left Pulmonary Arteries →
Lungs (Gas exchange in alveoli) → Oxygenated blood →
Pulmonary veins → Left atrium (receiving chamber) →
Bicuspid Valve → Left Ventricle → Aortic Semilunar Valve
→ Aortic arch → System/body

BLOOD CIRCULATION

How well did you know this?

Not at all

Perfectly

Blood Pressure (BP) is the force applied to walls of the
arteries. It is the force that moves through our circulation.

❖ BP is necessary because BP/blood is carrying essential
nutrients and oxygen needed for cellular and tissue life.
Additionally, BP does not only carry oxygen and nutrients
to nourish cells and tissues but it is vital because the
blood also delivers WBC and antibodies for immunity and
hormones including insulin.

Brief Review Ana/Physio

How well did you know this?

Not at all

Perfectly

What causes BP in our arteries?

This is because of our heart. Due to the force it delivers as it
contracts at each heartbeat.

How well did you know this?

Not at all

Perfectly

Cardiac Output (CO)
Peripheral vascular resistance (Compliance)

Determinants of BP

How well did you know this?

Not at all

Perfectly

amount of blood that flows from the heart through the ventricles, measured in Liters/min. (L/min.)

Cardiac Output (CO)

FORMULA FOR CO:

Stroke Volume (SV) x Heart Rate (HR) = CO

FACTORS AFFECTING CO

Elevation of CO by HR or SV Decrease of CO

● Catecholamines e.g. epinephrine, norepinephrine ● Thyroid Hormones ● Increase of Calcium ion levels

Elevation of CO by HR or SV

● Parasympathetic stimulation/stimulants ● Elevated/decreased levels of potassium ● Decrease in calcium levels ● Acidosis ● Anoxia - absence of oxygen

Decrease of CO

Ability of any compartment to expand or accommodate the increase of content For example, a balloon when not filled with air is small. When the balloon is inflated, it expands. The expansion done by the balloon is what we call _________

Peripheral vascular resistance (Compliance)

Whereas when compared to a metal, no matter how much one tries to break it, it will only bend and create an arch but will not totally follow the shape due to its ________________

Resistance

If there is ______ ___________ on the artery, the more effective it will be to expand and accommodate more blood as it surges.

Greater compliance

If it is capable of accumulating blood without difficulty or resistance, or no changes in BP, it is called as ____________

Peripheral Vascular Resistance.

_____ are more compliant than arteries because of its ability to expand and hold more blood.

Veins

Specialized cells in the arch of the aorta Sensors located in carotid sinuses and aortic arch. They are the ones that senses BP and the one that relays information to our brains so that there will be proper blood measure maintenance or homeostasis of blood pressure. From the blood (ventricles) it will pass into your aorta and carotid arteries and then if there’s sufficiency the baroreceptors will signal the brain so there’s homeostasis but if there’s alteration or insufficiency in the blood pressure your baroreceptors will also signal your brain so it will activate again.

Baroreceptors (pressure receptors)

● one of the mechanisms the body uses to maintain stable blood pressure levels or homeostasis. ● is a rapid negative feedback loop in which an elevated blood pressure causes heart rate and blood pressure to decrease. Reversely, a decrease in blood pressure leads to an increased heart rate, returning blood pressure to normal levels. ● The reflex starts with specialized neurons called baroreceptors. These are stretch receptors located in the wall of the aortic arch and carotid sinus. ● Increased blood pressure stretches the wall of the aorta and carotid arteries causing baroreceptors to fire action potentials at a higher than normal rate. These increased activities are sent via the vagus and glossopharyngeal nerves to the nucleus of the tractus solitarius – the NTS - in the brainstem. ● In response to increased baroreceptor impulses, the NTS activates the parasympathetic system – the PSNS - and inhibits the sympathetic system – the SNS. ● As the PSNS and SNS have opposing effects on blood pressure, PSNS activation and SNS inhibition work together in the same direction to maximize blood pressure reduction. ● Parasympathetic stimulation decreases heart rate by releasing acetylcholine which acts on the pacemaker cells of the SA node. ● Inhibition of the sympathetic division decreases heart rate, and stroke volume and at the same time causes vasodilation of blood vessels. Together, these events rapidly bring DOWN blood pressure levels back to normal. ● When a person has a sudden drop in blood pressure, for example when standing up, the decreased blood pressure is sensed by baroreceptors as a decrease in tension. Baroreceptors fire at a lower than normal rate and the information is again transmitted to the NTS. ● The NTS reacts by inhibiting parasympathetic and activating sympathetic activities. ● The sympathetic system releases norepinephrine which acts on the SA node to increase heart rate; cardiac myocytes to increase stroke volume and smooth muscle cells of blood vessels to cause vasoconstriction. Together, these events rapidly bring UP blood pressure levels back to normal. ● Baroreflex is a short-term response to sudden changes in blood pressure resulting from everyday activities and emotional states. ● If hypertension or hypotension persists for a long period, the baroreceptors will reset to the “new normal” levels. In hypertensive patients, for example, the baroreflex mechanism is adjusted to a higher “normal” pressure and therefore MAINTAINS hypertension rather than suppresses it.

Baroreflex or baroreceptor reflex

This particularly pertains to your kidney. The renin-angiotensin plays an important role in regulating your blood volume and your systemic vascular resistance may together influence your cardiac output as well as your arterial pressure In your renin persi is released primarily in the kidney. Responsible for the stimulation of angiotensin in your blood and your tissues. Once this one is stimulated it turns out that there will be stimulation in the release of aldosterone from your adrenal cortex. Renin persi is what we called a proteolytic enzyme that is released in our circulation from our kidneys.

RENIN-ANGIOTENSIN SYSTEM

three important components of RENIN-ANGIOTENSIN SYSTEM

1. Renin 2. Angiotensin 3. Aldosterone

PRIMARILY REASON WHY THERE IS A RELEASE OF RENIN Stimulated and secreted by:

1. sympathetic nerve activation 2. renal artery hypotension, (can be systemic hypotension and renal artery stenosis) 3. decreased sodium delivery in the distal tubule of the kidneys

Compensatory mechanism when blood pressure within the kidneys fall Primarily associated with blood pressure regulation by modulating blood volume, sodium reabsorption, potassium secretion, water reabsorption, as well as vascular code It is activated if there is a drop in the Blood Pressure or reduced blood flow/blood volume. There is now increased water and electrolyte reabsorption in the kidneys to compensate for decrease of blood flow so that it can lead to homeostasis/normalization of blood pressure.

Renin- Angiotensin Aldosterone System

Once there will be a decrease in blood pressure or oxygen, your juxtaglomerular cell or JG cell (kidney) is releasing the renin. When our renin is released, the angiotensinogen enzyme (liver) is also activated and it will be now stimulating angiotensin I with the presence of ACE inhibitors the angiotensin I will be converted into angiotensin II which is a potent vasoconstrictor. If there is vasoconstriction, your blood pressure will shoot up or there will be now an increase in blood pressure. A. If there is intense vasoconstriction there will be an increase in the peripheral resistance, as a result, the blood pressure will increase and there will be now the restoration of the blood flow or blood pressure and the kidneys now will be functioning well and there will be no decrease production of renin. B. the adrenal cortex will be stimulated to produce the hormone aldosterone. And from the nephrons, there will be sodium and water reabsorption so the sodium-rich blood will be retained in the body and the hypothalamus will be stimulated through the osmoreceptors and then this anti-diuretic hormones will be restricted from producing so that the blood pressure will increase or increase blood volume.

RAAS

The renin-angiotensin aldosterone system is a classic endocrine system that helps to regulate long-term blood pressure and extracellular volume in the body. The system begins with the release of angiotensinogen into circulation by the liver this may be in response to low blood pressure and adverse changes in sodium concentrations An enzyme renin is secreted which Cleaves angiotensinogen to form the inactive deca peptide angiotensin 1. Further, transformation of angiotensin is carried out by angiotensin converting enzyme or ace this is predominantly found in the pulmonary circulation. However, ACE is also produced in the vascular endothelium of many tissues including the kidney, adrenal gland, brain, and heart. The angiotensin converting enzyme converts the inactive precursor angiotensin one into the vasoactive peptide angiotensin ii. In addition alternative pathways exist that do not rely on either Rena or ACE. In non renin pathways enzymes like tonin and cathepsin d release angiotensin one from angiotensinogen and tissue plasminogen activator or TPA and can make angiotensin ii directly from angiotensinogen this bypasses the Midway production of angiotensin one. Enzymes like Chi May's can form angiotensin ii from angiotensin one via an ace independent pathway. Angiotensin converting enzyme also degrades bradykinin which is required for synthesis of a major vasodilator nitric oxide Angiotensin ii binds 81 receptors expressed on the surface of vascular endothelium and impairs nitric oxide synthesis as well. Reduced bioavailability of nitric oxide combined with the stimulation of 81 receptors on smooth muscle cells causes vasoconstriction. In addition to a vasoconstriction effect stimulation of 81 receptor causes the adrenal glands to release the hormone aldosterone resulting in sodium retention. Combined with vasoconstriction this increases blood pressure in the final stages of rass the kidney reduces the production of renin. Most of the known actions of angiotensin ii are mediated through the 81 receptors which can be found in the kidney, heart, vascular smooth muscle cells, brain, adrenal glands, platelets, adipocytes, and the placenta. angiotensin ii type 2 receptors can be found in low levels mainly in the uterus, adrenal, central nervous system, heart, and kidney. 82 receptors appear to counteract the effects of 81 receptor stimulation. another angiotensin ii type receptor is the 84 receptor it's stimulation may increase synthesis of the natural inhibitor of TPA called pi-1. Thereby reducing effective fibrinolysis stimulation of 84 receptor appears also to promote cell growth and proliferation

RAAS (video)

Also called as “silent killer” because not all people had symptoms It may precede heart attack, heart failure, stroke.

HYPERTENSION

TWO TYPES OF HYPERTENSION

1. Primary 2. Secondary

Also called as idiopathic hypertension. It will occur when you have abnormally high blood pressure that is not a result of a medical condition. Reversible: Diet, Exercise, Lifestyle modification, and compliance in medication Factors: Obesity, Family history, and unhealthy diet

Primary hypertension

Caused by another medical condition. It could be caused by a medical condition that pertains particularly affects the kidneys, arterys, heart, and endocrine system. It could also be caused by pregnancy

Secondary hypertension

Lifestyle modification - you need to change the way you live (excess is bad) ● Weight reduction ● Decrease sodium intake ● Moderate or cessation of alcohol intake ● Smoking cessation ● Increase physical exercise ● Take medication as prescribed

STEPS TO AVOID HYPERTENSION

P-ressure (blood) monitor R-ise slowly (may experience orthostatic hypotension - sudden drop of blood pressure) E-ating must be considered S-tay on medication S-kipping or abrupt stopping of medication is NO-NO U-ndesirable responses R-emind to exercise, decrease alcohol E-liminate smoking

HEALTH TEACHING

MOA: blocks the conversion of angiotensin I to angiotensin II Uses: Hypertension, MI Eg: - Benazepril (lotesin) - Moexipril (univasc) - Captopril (capoten) - Perindopril (aceon) - Enalapril maleate (vasotec) - Lisinopril - Quinapril (accupril) - Ramipril - Fosinopril (prinivil - Trandorapril SE: cough, hypotension, HA, dysgeusia (any perversion of taste perception), insomnia, N/V, diarrhea AE: reflex tachycardia, chest pain, angina, CHF, cardiac arrhythmias, ulcers, liver & renal problem, photosensitivity, hyperkalemia, neutropenia, angioedema - swelling underneath the skin specially in the airway and if there is obstruction in the airway the patient cannot breath DI: + probenecid = decrease elimination - It should not combine the ACE inhibitors and probenecid because it decreases the elimination in the incrition of the medication once it will metabolize. There are chances to have necrocicity if the ACE inhibitors and probenecid mix. + potassium supplement & diuretics =hyperkalemia - And if we combine our ACE inhibitor with potassium supplement as well as the diuretics we can have hyperkalemia. Where can we find hyperkalemia? Using our serum blood test, we can see their elevation in our electrolytes (eg. calcium, potassium) + NSAIDS = decrease hypotensive effect - ACE inhibitors should not be combined with NSAIDS because it might lose the hypotensive effect of the ACE inhibitors. + Antacids = decrease absorption - Just like other medications, we will not combine it with antacids because there will be alteration in the absorption. The antacids will cover the lining of the intestine, so the metabolism and absorption of the drug become slow. + Tetracycline = decrease absorption of tetra - Tetracycline cannot be mixed with ACE inhibitors because it might lose the drug effect of the tetracycline. CI: renal disease, severe Na depletion, CHF, pregnant and lactating women Nursing considerations - Encourage implement lifestyle changes - Administer on an empty stomach - Alert if patient is for surgery/dialysis/situations which may drop the fluid volume - Parenteral form only if oral form is not available - Adjust dose if with renal failure - Do not give if BP is below 90/70, monitor BP esp for 2 hours after the first dose (hypotension) - Avoid ambulation (dizziness) - Report cough/angioedema - Report dysgeusia if more than 1 month

ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (“pril”)

Selectively bind the angiotensin II receptors in the blood vessels and adrenal cortex Eg: - Telmisartan (Micardis) - Losartan (Diovan) - Irbesartan (Aprovel) - Candesartan (Blopress) - Valsartan (Cozaar) - Eprosartan (Teveten) USES: when ACE inhibitors are not tolerated SE: HA, diarrhea, dyspepsia, cramps AE: angioedema, hyperkalemia CI: nephro dysfunction, CHF, pregnancy Nursing considerations - +++ ensure female patient not pregnant - Take without regard to food

ANGIOTENSIN II RECEPTOR ANTAGONIST (“sartan”)

MOA: prevents movement of calcium ions in the myocardium and vascular smooth muscles. Normally: Ca increases muscle contractility, peripheral resistance and BP EG: amlodipine ( Norvasc) nimodipine (Nimotop) diltiazem (Cardizem) felodipine (Plendil) nicardipine ( Cardene) nifedipine (Procardia) verapamil ( Calan) USES: Angina, hypertension, atrial fibrillation SE/AD: HA, dizziness, hypotension, syncope, reflex tachycardia, constipation, AV block, bradycardia, peripheral edema Nursing considerations - Monitor ECG, CR, BP - Have “E” cart available with IV administration - Position to decrease peripheral edema - Protect drug from light and moisture - Increase OFI and fiber in the diet - Avoid overexertion when anginal pain is relieved - May give paracetamol if with HA - Take with meals or milk - No not chew or crush sustained released

CALCIUM CHANNEL BLOCKERS

MOA: relaxes smooth muscles of blood vessels esp the arteries; promotes increase blood flow to the brain & kidney EG: hydralazine ( Apresoline) minoxidil (Loniten) diazoxide ( Hyperstat) nitroprusside (Nitropress) USES: severe hypertension, emergencies SE/ AE: - hydralazine: tachycardia (beta blockers), palpitations, edema (diuretics), HA, dizziness, GI bleed, lupus like and neurologic symptoms - minoxidil: similar effects, excess hair growth, precipitates angina - Nitroprusside & diazoxide (hyperglycemia) : similar CI: allergy, pregnancy, lactation, cerebral insufficiency DI: + other antihypertensive drugs = additive effect Nursing considerations: - D – irectly acts on vascular smooth muscle - I – ncrease renal and cerebral blood flow - L – upus like reaction - A - ssess peripheral edema - T – ake with food - O – ther side effects - R – eview BP (orthostatic hypotension), blood glucose

VASODILATORS

A. BETA-ADRENERGIC BLOCKERS B. ALPHA-ADRENERGIC BLOCKERS C. CENTRALLY ACTING ALPHA2 AGONIST D. ADRENERGIC NEURON BLOCKERS (PERIPHERALLY ACTING SYMPATHOLYTICS) E. ALPHA1 & BETA1 - ADRENERGIC BLOCKERS

SYMPATHOLYTIC DRUGS

BETA- BLOCKERS “OLOL” ■ beta-adrenergic blocking agents,beta-adrenergic antagonists, beta antagonists.

SYMPATHOLYTIC DRUGS

MOA: block beta 1 (Cardiac) and / or beta 2 (lungs) adrenergic receptor sites; decrease the effects of the SNS by blocking the release of catecholamines, thereby decreasing the HR and BP USES: hypertension, dysrhythmias, angina pectoris AE: rebound hypertension Main contraindications (ABCDE) * A- sthma * B- lock (heart block) * C- OPD * D- iabetes mellitus * E- lectrolyte imbalance (hyperkalemia) DI: + antacids = delayed drug absorption + lidocaine = increase plasma level of lidocaine + insulin/ OHA= hypo/hyperglycemia + cardiac glycosides= additive bradycardia + calcium channel blockers= increase pharmacologic and toxic effects of both + cimetidine= decrease metabolism of beta blockers + theophylline = mpaired bronchodilating effect Eg: Nonselective Beta Blockers * Carvedilol ( Coreg) * Nadolol ( Corgard) * Propranolol ( Inderal) * Timolol ( Blocadren) * Pindolol ( Visken) Cardioselective Beta Blockers (B1) * acebutolol (Sectral) * atenolol ( Tenormin) * betaxolol ( Kerlone) * bisoprolol (Zebeta) * esmolol (Brevibloc) * metoprolol (Betaloc, Cardiostat) ➔ Nursing considerations - Lifestyle modification; Compliance ( rebound hypertension) - Monitor blood sugar with diabetes - Monitor triglycerides and cholesterol level (LDL) - Monitor BP & pulse before and after - Withhold if pulse is < 60 or SBP < 90 - Monitor any change in the rhythm or signs of CHF BLOCKER B- radycardia L- ipidemia increases - libido decreases br O - nchospasm C- HF - onduction abnormalities K- onstriction peripheral vascular E - xhaustion - motional depression R - educes recognition of hypoglycemia “BLOCKER” outlines undesirable effects of beta blockers

A. BETA-ADRENERGIC BLOCKERS

are found in the heart and kidneys. When stimulated, they increase heart rate, AV conduction, & automaticity

Beta-one receptors

reduce heart rate, blood pressure, myocardial contractility, and myocardial oxygen consumption.

Beta1-blockers

mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. serve to dilate bronchial & vascular smooth muscle.

Beta-two receptors

inhibits relaxation of smooth muscle in blood vessels, bronchi, the gastrointestinal system, and the genitourinary tract.

Beta2-receptor blockade

MOA: blocks alpha 1 adrenergic receptors resulting in vasodilation of arteries and veins Decrease peripheral resistance; relaxes smooth muscle of bladder / prostate Decrease VLDL & LDL = decrease fat deposits ; increase HDL Does not affect glucose metabolism & respiratory function Causes Na & H2O retention with edema; given with diuretics WARNINGS: renal disease, elderly more sensitive EG: ● Potent Alpha Blockers: hypertensive crisis & severe hypertension from catecholamine secreting tumors of the adrenal medulla (pheochromocytoma) - Phentolamine - Phenoxybenzamine - Tolazoline ● Prazosin (minipress) = CHF ● Doxazosin (cardura) = also for BPH ● Terazosin (hytrin) = also for BPH SE: - orthostatic hypotension (dizziness, faintness, increase HR) - 1st dose syncope (hypotension with loss of consciousness) - Nausea, drowsiness, nasal congestion, weakness, loss of libido - Phentolamine – reflex tachycardia DI: - + other antihypertensive, alcohol, nitrates = increase hypotensive effects - Prazosin + anti inflammatory drug = peripheral edema - Prazosin & nitroglycerin = syncope Nursing interventions - Monitor BP frequently - Protect from falling / injury - Assess BP and HR before each dose - If dose is during the day, client must remain recumbent for 3-4˚ - Assist with ambulation if client is dizzy Education - Implement safety precautions - Report if edema is present - Sugarless gum, sips of tepid H2O, etc. may relieve dry mouth Mini’s SINS S - yncope - exual dysfunction I - ncreased drowsiness, orthostatic hypotension, HR N - eed to be recumbent for 3-4 hours after initial dose Mini’s “SINS” (minipress) are undesirable effects of alpha adrenergic blockers. These medications end in SIN.

ALPHA-ADRENERGIC BLOCKERS

MOA: decrease sympathetic response from brainstem to the peripheral vessels; resulting in a decrease peripheral vascular resistance & BP Stimulate the alpha2 receptors: ■ Decrease sympathetic activity ■ Increase vagus nerve ■ Decrease epinephrine, norepinephrine, renin release SE/ AE: drowsiness, HA, dry mouth, dizziness, bradycardia, constipation, hypotension, occasional edema or weight gain DI: paradoxical hypertension with propranolol EG: - Methyldopa (Aldomet) (chronic / PIH) *** - Clonidine (Catapres)*** *** cause Na & water retention (given with diuretics) Nursing considerations - Monitor baseline VS ( q30 mins until stable during initial therapy) & weight ( refer: wt gain > 4 lbs/ week) - Abrupt D/C = hypertensive crisis ( restlessness, tachycardia, tremors, HA, & increase BP), compliance - Taper dose gradually over more than one week - Recommend the last dose of the day to be taken at bedtime - Sugarless gum, sips of tepid water may relieve dry mouth

CENTRALLY ACTING ALPHA2 AGONIST

MOA: block norepinephrine release from the sympathetic nerve endings that results in decrease BP SE: orthostatic hypotension, Na & water retention vivid dreams, nightmares & suicidal intention (reserpine) EG: - reserpine (Serpasil) - guanethidine monosulfate (Ismelin) Nursing considerations - Take with meals, no alcohol

ADRENERGIC NEURON BLOCKERS (PERIPHERALLY ACTING SYMPATHOLYTICS)

MOA: blocks both alpha1 and beta1 receptor sites; decrease BP & moderately decrease PR SE: orthostatic hypotension, GI disturbances, nervousness, dry mouth, fatigue AE: heart block CI: large doses could block beta 2 receptors = increase airway resistance in patients with asthma Eg: - labetalol (Normodyne) - carteolol (Cartrol)

ALPHA1 & BETA1 - ADRENERGIC BLOCKERS

Forms of antibiotics that has similar spectrum although they differ in structure Includes vancomycin, lincosamides, ketolides Also includes antibiotics such as erythromycin, azithromycin, clarithromycin, and proximothrycin Indications: - Mild to moderate infections of the RT - Sinuses - GIT - Skin & soft tissues - Diphtheriae - Impetigo - STD *also used as an alternative treatment for patients who have allergies to antibiotics such as penicillin and cephalosporins Interfere with the protein synthesis of the bacteria and their function depends on the concentration and type of the bacterial species Can be both bacteriostatic (inhibit the growth of the bacteria) and bactericidal (kill the pathogen) Effective against gram positive, but excluding your enterococci bacteria and some gram negative bacterias Common first-line indications for macrolides

MACROLIDES

1. ERYTHROMYCIN (1950s) (Erythrocin, Erymax)

MACROLIDES

derived from Streptomyces erythreus most commonly prescribed if with allergy to PCN ♦ effective against gram (+) and some gram (-) except S. aureus DRUG OF CHOICE: > Mycoplasma Pneumoniae > Legionnaires disease - Prevention of rheumatic fever PC: B (no risk evident) MOA: inhibits CHON synthesis, BACTERIOSTATIC (low dose)/BACTERICIDAL (high dose) Contraindications: Hepatic disease (aggravate more the problem of the pt), Lactation (could pass on your breastmilk barrier) PHARMACOKINETICS - PO form is well-absorbed in the duodenum (erythromycin is easily inactivated by the gastric acid - oral formulation of erythromycin are in intericoated or in immerse stable salt or esters) - Acid resistant salts (Ethylsuccinate stearate, estolate) > decrease the dissolution of erythromycin, increasing the absorption of this medication on the intestine. Food will not hamper the absorption of acid resistant macrolide) Route of administration: > Oral > No IM; preferably slow IVTT (patient might have phlebitis if not slow) > No IM because it is irritant to the muscles Protein bound: 65% T ½ : PO (1-2hr) [estimated time it takes for the concentration or the amount in the body of the drug to be reduced exactly half] Excreted: through bile (normal liver function), feces, and small amount through the urine (5% of the medication if orally administered) PHARMACODYNAMICS - Orally administered > Onset : 1hr > Peak : 4hrs > Duration : 6hrs SE: - N&V, diarrhea, loss of appetite - Pruritus, rash - Tinnitus AE: - Superinfections - Urticaria - Hearing loss - Hepatotoxicity (yellow sclera) - Anaphylaxis Drug interactions - Acetaminophen, phenothiazine, sulfonamide (decrease the metabolism - leading to increase risk of hepatotoxicity) - Digoxin, carbamazepine, theophylline, cyclosporine, warfarin, triazolam (increase in the effectivity of drugs and serum concentration - good effect) - PCN, clindamycin (decrease in the therapeutic efficacy) - Antacids (alter absorption because antacids cover the intestinal lining - once covered, slower time for the meds to absorb - absorption will decrease) - Verapamil, diltiazem, clarithromycin, fluconazole (elevation of erythromycin concentration - higher risk for severity of adverse effects - might lead to cardiac arrest)

ERYTHROMYCIN (1950s) (Erythrocin, Erymax)

Broad spectrum type of macrolide ; has a long half life; has a high degree of tissue penetration Indications - Mild-moderate streptomycin infection - RTI - Gonorrhea - Chancroid (STD) - H. influenzae, - Strep. - S. aureus Pregnancy category: - C (can’t be ruled out) Absorption: - Not affected by food - PO - once a day x 5 days incompletely absorbed in the GIT - There should be compliance Distribution: - Measure in tissues rather than plasma/serum - T ½ : 40-50 hrs; only 37% (bioavailability) reaches in the systemic circulation - Should not be given to pt’s who have hepatic/kidney problems Excretion: bile, feces, & urine (less) SE (uncommon) - Nausea and vomiting - Diarrhea - Loss of appetite (Nsg. Mgt.: Give drug 1hr ac or 2hr pc + 1 glass of water not fruit juice) IV PREP: - Must be diluted in NSS (to prevent phlebitis)

AZITHROMYCIN (ZITHROMAX)

Usually used for the treatment of wide variety of bacterial infections Acute otitis, pharyngitis, tonsillitis Indications: - RTI - Gram (-) & (+) - Tissue infections - H. pylori Pregnancy category: - C (can’t be ruled out) Absorption: PO - Well absorbed in the GI tract - Taken with food Distribution: T ½ : 3-6hrs - Thoroughly distributed all throughout the body and achieves its higher concentration in the tissues than in the blood Metabolism: PB = 65-75% - Undergoes extensive first pass metabolism (phenomenon in which the drug gets metabolized at a specific location) Excretion: bile and urine SE: - Nausea and vomiting - Diarrhea - Loss of appetite (Nsg. Mgt.: Take drug with meal/milk)

CLARITHROMYCIN (KLARICID)

Respiratory, skin, and other types of infection Indications: - Chronic bronchitis - URTI - CAP - Skin infections - H. Pylori - Legionnaires disease - Chlamydia Pregnancy category: - C (can’t be ruled out) Absorption: PO - Absorbed in the GIT Distribution: T ½ : 20-50hrs Metabolism: Unknown (PB) - 60-90% of the dose is hydrolyzed within 30min after it is ingested; it will take 1 ½ hour before the drug to be totally converted and absorbed/metabolized; undergoes little or no hepatic biotransformation - Excretion: Bile and urine SE (common): - Nausea and vomiting - Diarrhea - Loss of appetite (Nsg. Mgt.: Take with food, or within 1hr of eating)

DIRITHROMYCIN (DYNABAC)

- Do not refrigerate suspension form of clarithromycin (disrupt the chemical component - potency - structure) - Monitor liver enzymes – signs & symptoms of hepatotoxicity - Administer IV slowly - Give IM into deep muscle (not really considered) - Avoid fruit juices - Manage NAVDA (small frequent feeding;1hr or 2hr before/after meal) Check for superinfections. Give yogurt/buttermilk (alter the superinfections) - Check drug interactions - Evaluate effectiveness: WBC level, temperature, cultures The macrolide girl G - GI disturbances (undesirable effects) I - IV site (check irritation) R - reduces activity of med if given with acids (fruit juices) or food L - liver function test

Nursing care for patients taking macrolides

A. CLINDAMYCIN (CLEOCIN) B. LINCOMYCIN (LINCOCIN) C. VANCOMYCIN HCI (VANCOCIN) D. FLUOROQUINOLONES

LINCOSAMIDES

Lincomycin, clindamycin, premalycine Used to prevent bacterial replication in bacteriostatic mechanism It will just not inhibit the growth, but prevent the replication of the pathogens through interfering with the protein synthesis Similar with the macrolides, but lincosamides are more toxic Change protein function and prevent cell division and cause cell death, or both

LINCOSAMIDES

Widely prescribed against most gram (+) organism; absorbed better, more effective, lesser toxic For severe infections caused by the same strains of bacteria that are susceptible to macrolides Pregnancy category: B; only if benefit clearly outweighs risk Absorption: rapidly absorbed from GIT and from IM injections Distribution: T ½ = 2-3hrs Protein bound: 94%; crosses the placenta & enters breastmilk Metabolism: liver (caution: hepatic & renal impairment) Excretion: urine & feces SE: - GI reaction (pseudomembranous colitis (antibiotic associated colitis - inflammation of the colon with an outgrowth of bacterium clostridiosis deficine - connected to hospital stay or antibiotic treatment - common to people who are > 65yrs old ; GI irritation)

CLINDAMYCIN (CLEOCIN)

An antibiotic that is indicated only for the treatment of serious infections and is typically reversed for use in cases of penicillin allergy or where penicillin is inappropriate Very potent Absorption: rapidly absorb in GIT or from IM injections Distribution: T ½ = 5hrs Metabolism: liver (caution: hepatic & renal impairment) Excretion: bile and urine Toxic effects: GI reaction, pain, skin infection, BM depression Nursing care: Same with macrolides - Careful monitoring - GI activity & fluid balance - Stop if with bloody diarrhea (severe effect)

LINCOMYCIN (LINCOCIN)

A glycopeptide antibiotic medication that is usually used to treat a number of bacterial infection Usually given intravenously as treatment for complicated skin infection, blood stream infection, as well as endocarditis, and bone and joint infections Also used for patient who have meningitis caused by methicillin resistant staphylococcus aureus Usually used for treatment of serious and life threatening infections caused by gram (+) bacteria (last resort because this is abandoned since it is very potent or isog na kaayo siya. The pt is prone to have a systemic problem if given with vancomycin) Almost abandoned (The pt is prone to have a systemic problem if given with vancomycin. Pt is also prone to nephrotoxicity and ototoxicity - damage of cranial nerve 8) Glycopeptide bactericidal antibiotic Mode of action: - Bactericidal: inhibits bacterial cell wall synthesis PB: 30% Half-life: 6hrs ORAL - not absorbed systemically (put into waste) - Excreted in feces - Treatment for severe clostridium difficile colitis INTRAVENOUS - For severe infections due to MRSA, septicemia, bone, skin and lower respiratory tract infections that are resistant to other antibiotics - Give very slow - Excreted in urine - This is not absorbed in your intestines. Has also a short half-life that is why it is given IV for 2 times a day. Usually a single dose. Drug interactions: - Amphotericin B, polymycin, furosemide, cisplatin (diuretics - pt might have nephrotoxicity) - Methotrexate (pt might have methotrexate toxicity) SE & AE: - Chills - Nausea - Dizziness - Vomiting - Fever - Thrombophlebitis @ injection site - Rashes Dose related toxicity - Tinnitus - High tone deafness - Hearing loss - nephrotoxicity Rapid IV infusion “red-neck or red man syndrome” (vancomycin flushing reaction) - Reaction appears 4-10 mins after the vancomycin is administered - Pt will have a flushing or erythematous rash that is usually found on the face, neck, or upper torso. This is attributed due to the release of histamine from the mast cells - Symptoms of red man syndrome can be treated or prevented if you are going to administer antihistamine such as diphenhydramine. Nursing care: - Refrigerate IV solution after reconstruction, use within 96hrs - Flush IV line in between antibacterials. Evaluate IV site for phlebitis, avoid extravasation (burn & blister). - Ensure safety - Check baseline hearing. Refer to ENT. Report ringing in ears or hearing loss, fever and sore throat. - Monitor blood pressure during administration - Monitor renal function tests-creatinine, BUN, and urine output; and liver enzymes (bile & feces) - Yogurt for superinfection (eating yogurt could replace good bacteria that could help maintain the correction of balance and keeping the yeast from overgrowing) - Check for pregnancy & lactation (Pregnancy category B and C - considered safe to use during pregnancy when there are no any other medications given to the pt, but, it falls to category C because there is no confirmation that it is safe for the fetus) Rudolf the Red - Neck reindeer Rudolf the red-neck reindeer Had an adverse side effect From the drug vancomycin Must keep all labs in check Caution with renal failure, Hearing loss and allergies, Take a temp and blood cultures, Especially the CBC!!

VANCOMYCIN HCI (VANCOCIN)

Represent an evolving class of broad spectrum antimicrobial agents that is used in the prevention and treatment of ocular infections Ciprofloxacin, gemifloxacin, levofloxacin, moxifloxacin, and ofloxacin Mode of action: - Interfere with the enzyme DNA gyrase (needed to synthesize bacterial DNA) - Broad spectrum bactericidal Considerations before taking the drug: - Allergies (cinoxacin > hypersensitivity reaction=anaphylactic shock) - Pregnancy (contraindicated - there will be fetal malformation - bone defect) - Breast-feeding (has the ability to pass on human breast milk) - Children (< 18yrs old, not advised to take fluoroquinolones because there will be a high chance of bone deformity and growth spurt) - Older adults (have been tested and seen effective result and has not shown to cause any side effects or problems) - Other medicines (make cause alteration and may completely interfere with the metabolism of other drugs including theophylline and aminophylline) - Other medical problems (the presence of other medical problems may affect the use of fluoroquinolones) >[brain or spinal cord disease, seizure attacks, history of epilepsy = may cause nervous system side effects that can trigger seizure activities] > [not allowed to give to DM pt (levofloxacin) cause it may cause changes in blood sugar and results to difficulty to manage blood sugar] > _________ rabies (muscles disease) = the condition of pt may worsen which causes respiratory muscle to become weak and life threatening (DOB) MEDS - Nalidixic acid (negram)/cinoxacin (cinobac) > Prescribed primarily for UTI by gram (-) E.coli, LRTI, skin, soft tissue, bone & joint infxns - Ciprofloxacin (cipro)/Norfloxacin (noroxin) > Broad spectrum including P. aeruginosa - Levofloxacin (levaquin)/Sparfloacin (zagam)/Trovafloxacin (trovan) > Treat respiratory problems CAP, chronic bronchitis, acute sinusitis, UTI, and skin infections > Absorbed from GIT, low PB, moderately short half-life, 75% excreted in the urine - Gatifloxacin (tequin)/Moxifloxacin (avelox) > OD dosing more active than levofloxacin against S. pneumoniae SE Photosensitivity - use sunglasses, sunblock, protective clothing - Dizziness - N/V - Diarrhea - Flatulence - Abdominal cramps - Tinnitus - Rash Nursing management: - Assess renal function : I/O, BUN, creatinine (essential to determine if pt is having nephrotoxicity) - Drug & diet history: > Avoid caffeine (increase nervousness, sleeplessness, palpitations, increase in anxiety) > Antacids & iron prep (decrease the absorption of the antibiotic) > Monitor serum theophylline & blood glucose (increase in their effects = uncontrolled sugar level) > Use of NSAIDS (seizure attack because it triggers CNS reaction) > Administer 2hrs ac or after antacids (absorption are impaired when combined with antacids [aluminum & magnesium] > With iron preparation (alter and decrease its effectivity of the antibiotic) [full glass of water] > IV dose (infused over 30 mins) - very slow administration since it irritates - dilute it with approximate amount of NSS to avoid phlebitis and damage of vessels or wall of the veins - Check S/S of superinfections (stomatitis, furry black tongues, genital discharges, itchiness) - Check symptoms of CNS stimulations (trigger CNS activity - nervousness, insomnia, anxiety, tachycardia)

FLUOROQUINOLONES

- Another type of broad spectrum drugs - “Sulfa drugs” - One of the oldest antibacterial agents; when PCN (miracle drug) - Chemically man-made/synthetic med - 1st isolated from a COAL TAR (dye) derivative compound in early 1900; produced for clinical use against coccal infections in 1935 - 1st group of drugs used against bacteria - Not classified as an antibiotic because they were not obtained from biological substances MOA: - Inhibit bacterial synthesis of FOLIC ACID, essential for bacterial growth, necessary for synthesis of PURINE & PYRIMIDINES, which are precursors of RNA & DNA - Considered as bacteriostatic - Dihydropteroate - For cells to grow and reproduce, they required folic acid; humans cannot synthesize FA but depend on folate from the diet. Bacteria are impermeable to FA & must synthesize it inside the cell. - Remain inexpensive & effective against UTI, trachoma, ear infection, newborn eye prophylaxis - 90% effective against E.coli; useful in treatment of meningococcal meningitis & against organisms Chlamydia & Toxoplasma gondii; not effective against viruses & fungi - If combined with trimethoprim = bactericidal effect ang sulfonamide PHARMACOKINETICS [A] well absorbed by the GIT [M] liver [D] well distributed to body tissues and brain [E] urine PHARMACODYNAMICS - Many for ORAL administration - Also in solution & ointment for ophthalmic use and in cream form = SILVER SULFADIAZINE (silvadene) and MAFENIDE ACETATE (sulfamylon) - Most - highly protein bound & displaced other drugs by competing for CHON sites NOTE: - Apply ointment into the eyes of the baby to avoid infections - Apply to burned pt/victims of burn

SULFONAMIDES

2 CLASSIFICATIONS OF SULFONAMIDES

1. SHORT ACTING 2. INTERMEDIATE

1. SULFADIAZINE 2. SULFISOXAZOLE (Gantrisin)

SHORT ACTING SULFONAMIDES

- Oral agent with broad spectrum use - Slowly absorbed from GIT, peak 3-6 hr - Poorly soluble in urine, cause crystallization; can damage kidneys if water is less introduced after taking the med - Should not be used in infants under 2 mos old (oral/IV) - Rheumatic fever & Meningococcal meningitis SIDE EFFECTS & ADVERSE REACTIONS: (SE) - Nausea - Vomiting - Diarrhea - Loss of appetite - Headache (AR) - mental/mood changes - Signs of kidney prob. (pain in urination - decrease of urine) - lump/growth/swelling in the front of the neck (goiter) - Signs of low blood sugar (shaking, dizziness, blurred visions, feeling of hunger, hypoglycemia)

SULFADIAZINE

- Broad spectrum - Recommended by CDC for treatment of STD - Useful with Sulfadiazine in prophylactic treatment of streptococcal infection - rheumatic fever - Also given to pt who have hypersensitivity of penicillin - Rapidly absorbed from GIT - Peek 2 hrs - Excreted in urine, t ½ = 4.5 - 7.8 hrs INDICATIONS: - Treatment of severe, repeated, or long-lasting UTI - Meningococcal meningitis - Acute otitis media (ear infection) - Trachoma - Inclusion conjunctivitis - Nocardiosis - Chancroid - Toxoplasmosis - Malaria

SULFISOXAZOLE (Gantrisin)

1. SULFAMETHOXAZOLE (Gantanol/SMZ/SMX) 2. SULFASALAZINE (Azulfidine) 3. COTRIMOXAZOLE (Septa, Bactrim)

INTERMEDIATE ACTING SULFONAMIDES

- Poorer water solubility than Sulfisoxazole MOA: - Inhibiting the production of dihydrofolate intermediate interferes w the normal bacterial synthesis of folic acid (folate - Blockage of folate production PHARMACOKINETICS: Absorbed - well-absorbed when administered topically & rapidly absorbed when orally administered Distribution 1. Distributed into most body tissues as well as into sputum, vaginal fluid, and middle ear fluid 2. Also crosses the placenta 3. Plasma protein bound: 70% 4. Max. drug concentration: occurs 1-4 hrs after oral adm. 5. Serum half-life: 10 hrs Metabolism: - Sulfamethoxazole is metabolized in the human liver to at least 5 metabolites. 1. N4-acetyl2. N4-hydroxy3. 5-methylhydroxy4. N4-acetyl-5-methylhydroxy 5. N-glucuronide conjugate SIDE EFFECTS & ADVERSE REACTIONS: (SE) - Gastrointestinal disturbances (nausea & vomiting; loss of appetite = Nsg. mgt: SFF) - Allergic skin reactions (rash, urticaria) (AR) - Stevens-Johnson syndrome (SJS) - Toxic epidermal necrolysis - Hepatic necrosis - Agranulocytosis - Aplastic anemia

SULFAMETHOXAZOLE (Gantanol/SMZ/SMX)

- Used to treat ULCERATIVE COLITIS & CROHN’S disease; triumatic arthritis - Carried by AMINOSALICYLIC ACID (aspirin) - Rapidly absorbed from GIT - Peak levels 2-6 hrs - Metabolized in the liver - Excreted in urine; t ½ = 5-10hrs MOA: - Inhibition of prostaglandins, resulting in local antiinflammatory effects in the colon. SIDE EFFECTS & ADVERSE EFFECTS: - Loss of appetite - Nausea - Headache - Rash - Skin and urine can become orange (AR) - Bone marrow suppression - Liver problems - Stevens-johnson syndrome - Kidney problems

SULFASALAZINE (Azulfidine)

Combination drug of Sulfamethoxazole & trimethoprim (synergistic effect = interactions of 2 drugs that is producing a greater sum effects) Effective in treating otitis media, bronchitis, UTI and pneumonitis by Penucystic Carinii DOC: Penumocystis Carinii Pneumonia (PCP) Infused over 60-90 mins; no IM (bcoz it comes in large amount & irritating; given via infusion) - [A] rapidly from the GIT (orally); peak 2 hrs - [M] liver (oral) - [E] urine; t ½ = 7-2 hrs (oral) PC: - category D (contraindicated) - Teratogenic - birth defects - Kernicterus ( brain damage); Breastmilk = diarrhea & rash on infant THERAPEUTIC ACTION: - Competitively block PARA-AMINOBENZOIC ACID (PABA) to prevent synthesis of folic acid in susceptible bacteria that synthesize their own folates for production of DNS & RNA (SE) - Rash, itching - BLOOD: hemolytic anemia, aplastic anemia, pancytopenia (prolonged & high dosages) = due to BM depression - GI: anorexia, N/V {mgt: SFF} - CRYSTALLURIA (crystals in urine); hemturia (sulfonamides are insoluble in acid urine) {increase OFI = dilutes the drug} (AR) - Photosensitivity {avoid sunbathing & excess UV light} - Cross-sensitivity - with diff. Sulfonamides - Hepatoxicity & nephrotoxicity - Superinfections {frequent oral care, ice chips, sugarless candy = to relieve discomfort}; yogurts (increased the proliferation) - Hypersensitivity reaction = STEVEN’S JOHNSONS SYNDROME {discontinue drug} - CNS effects: HA, dizziness, vertigo, ataxia, convulsions, depressions {due to effect to nerves} DRUG INTERACTIONS: - Increase effects of Warfarin - Decrease absorption if taken w antacids - Increase hypoglycemic effects of sulfonylureas (feeling weak; hunger) - Decrease effectiveness of contraceptives NURSING CARE: - Baseline S. crea, BUN, urine output (should be 1,200 ml/day) - Increase OFI - 2,000 ml/day or >; administer with full glass of H2o - Baseline CBC, liver enzymes (AST, ALT, alkaline phosphatase); monitor for jaundice, icteric sclera (puti sa mata turned yellowish = hepatic prob/jaundice) - Monitor VS, check for fever & bleeding - Observe for hematologic reaction that may lead to life-threatening anemias; monitor signs of sore throat, purpura - Check for signs of superinfections - Administer 1 hr ac or 2 hrs pc with 1 glass of water - avoid /limit sun exposure, use sunblock - Use clinistix to monitor urine sugar & ketones in diabetic pt (not clinitest tab) - Not to be taken with antacids - Avoid during last trimesters of pregnancy S = unlight sensitivity U = undesirable effects = RASH, RENAL TOXICITY L = ook for urine output, fever, sore throat & bleeding F = luids galore A = norexia, anemia

COTRIMOXAZOLE (Septa, Bactrim)

1. CHLORAMPHENICOL (Chloromycetin) 2. SPECTINOMYCIN HYDROCHLORIDE (Trobicin) 3. QUINUPRISTIN / DALFOPRISTIN (Synercid) 4. PEPTIDES

UNCLASSIFIED ANTIBACTERIAL DRUGS

2 TYPES OF PEPTIDES

a. POLYMYXIN b. BACITRACIN

Discover in 1947 - MOA: BACTERIOSTATIC = inhibits bacterial protein synthesis - SPECTRUM: BROAD = especially against ricketssiae, mycoplasma, H. influenzae - USES: serious infections of SKIN, SOFT TISSUE, CNS infections - including meningitis, ophthalmic infections — when less toxic drugs cannot be used; t ½ = 1.5 - 4 hrs PC: C PB = 50 - 60% SE: - BM depression = blood dyscrasias - NEURO = confusion, peripheral neuritis, depression - GRAY SYNDROME = in newborn characterized by abdominal distention, vomiting, pallor, cyanosis; NB may die due to immature liver function NURSING CARE: - Monitor infection, bleeding - Monitor for anemia, CBC - Monitor LOC

CHLORAMPHENICOL (Chloromycetin)

Introduced in 1971 against Neisseria gonorrhea (GONORRHEA) Allergic to PCN, Cephalosporins, Tetracycline Administered IM single dose = BACTERIOSTATICS PC: B; PROTEIN BOUND = 10%; t ½ = 1-3 hrs

SPECTINOMYCIN HYDROCHLORIDE (Trobicin)

- Treat VREF = Vancomycin-resistant Enterococcus faecium bactermia & skin Infected by S. eus & S. pyrogenes - Disrupts CHON synthesis of the organism - When administered through peripheral IV line = PAIN, EDEMA & phlebitis - SE: N/V, diarrhea, pseudomembranous colitis, headache, anaphylaxis, elevated AST & ALT SPECTINOMYCIN HYDROCHLORIDE (Trobicin); QUINUPRISTIN/DALFOPRISTIN (Synercid) - Check for DHN, monitor stools - Check for patency of IV line; infuse over 1 hr in D5W - Check for S/S of anaphylaxis - Monitor ALT, AST, jaundice, icteric eyes - Give ice chips, SFF

QUINUPRISTIN / DALFOPRISTIN (Synercid)

Derived from cultures of bacillus subtilis

PEPTIDES

- Interferes with cellular membrane - Bactericidal - Affects gram (-) like E. coli, P. aeruginosa, klebsiella, shigella - Not absorbed orally - IM cases pain - Best given slow IV - SE: dizziness - AE: nephrotoxicity/neurotoxicity

POLYMYXIN

- Inhibits cell wall synthesis - bactericidal/bacteriostatic - Most gram (+), some gram (-), can treat meningitis - Not absorbed by GIT - Given IM/IV - SE: N/V - AE: nephrotoxicity, respiratory paralysis, blood dyscrasia, anaphylaxis

BACITRACIN