DRUGS AFFECTING THE CARDIOVASCULAR SYSTEM Flashcards

1
Q

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

A

ANTIHYPERTENSIVES

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2
Q

What do we particularly prevent if we have
hypertension?

A

Stroke and myocardial infarction

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3
Q

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

A

Antihypertensives

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4
Q

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.

A

DIURETICS

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5
Q

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.

A

Diuretics notes

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6
Q

○ Thiazide
○ Osmotic
○ Loop
○ Potassium-Sparing

A

Diuretics

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7
Q

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

A

ANTI- ANGINAL

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8
Q

○ Nitrates
○ Non-nitrates

A

ANTI- ANGINAL

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9
Q

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.

A

Arrhythmia

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10
Q

defibrillator is used to bring shock to the heart

A

Flatline or asystole

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11
Q

➢ Atrial Fibrillation
➢ Ventricular Fibrillation
➢ Atrial Flatters

A

IRREGULARITIES IN ECG TRACING

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12
Q

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.

A

IRREGULARITIES IN ECG TRACING NOTE

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13
Q
  • 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.
A

CARDIAC GLYCOSIDES

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14
Q

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

A

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

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15
Q
  1. Anticoagulants
  2. Thrombolytics
A

DRUG AFFECTING THE BLOOD

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16
Q

(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

A

Anticoagulants

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17
Q

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

they are used to dissolve clots

A

Thrombolytics

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18
Q

How are thrombolytics different from anticoagulants?

A

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.

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19
Q

➢ 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

A

Hemostatics

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20
Q

❖ 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

A

ANATOMY OF THE HEART

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21
Q

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

A

BLOOD CIRCULATION

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22
Q

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.

A

Brief Review Ana/Physio

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23
Q

What causes BP in our arteries?

A

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

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24
Q

Cardiac Output (CO)
Peripheral vascular resistance (Compliance)

A

Determinants of BP

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25
Q

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

A

Cardiac Output (CO)

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26
Q

FORMULA FOR CO:

A

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

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27
Q

FACTORS AFFECTING CO

A

Elevation of CO by HR or SV
Decrease of CO

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28
Q

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

A

Elevation of CO by HR or SV

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29
Q

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

A

Decrease of CO

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30
Q

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 _________

A

Peripheral vascular resistance (Compliance)

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31
Q

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 ________________

A

Resistance

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32
Q

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

A

Greater compliance

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33
Q

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

A

Peripheral Vascular Resistance.

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34
Q

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

A

Veins

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35
Q

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.

A

Baroreceptors (pressure receptors)

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36
Q

● 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.

A

Baroreflex or baroreceptor reflex

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37
Q

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.

A

RENIN-ANGIOTENSIN SYSTEM

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38
Q

three important components of RENIN-ANGIOTENSIN SYSTEM

A
  1. Renin
  2. Angiotensin
  3. Aldosterone
39
Q

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

A
  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
40
Q

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.

A

Renin- Angiotensin Aldosterone System

41
Q

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.

A

RAAS

42
Q

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

A

RAAS (video)

43
Q

Also called as “silent killer” because not all
people had symptoms

It may precede heart attack, heart failure, stroke.

A

HYPERTENSION

44
Q

TWO TYPES OF HYPERTENSION

A
  1. Primary
  2. Secondary
45
Q

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

A

Primary hypertension

46
Q

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

A

Secondary hypertension

47
Q

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

A

STEPS TO AVOID HYPERTENSION

48
Q

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

A

HEALTH TEACHING

49
Q

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

A

ANGIOTENSIN-CONVERTING ENZYME
INHIBITORS (“pril”)

50
Q

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

A

ANGIOTENSIN II RECEPTOR ANTAGONIST
(“sartan”)

51
Q

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

A

CALCIUM CHANNEL BLOCKERS

52
Q

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

A

VASODILATORS

53
Q

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

A

SYMPATHOLYTIC DRUGS

54
Q

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

A

SYMPATHOLYTIC DRUGS

55
Q

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

A. BETA-ADRENERGIC BLOCKERS

56
Q

are found in the heart and kidneys.

When stimulated, they increase heart rate, AV
conduction, & automaticity

A

Beta-one receptors

57
Q

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

A

Beta1-blockers

58
Q

mainly in the lungs, gastrointestinal tract, liver, uterus,
vascular smooth muscle, and skeletal muscle.

serve to dilate bronchial & vascular smooth muscle.

A

Beta-two receptors

59
Q

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

A

Beta2-receptor blockade

60
Q

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.

A

ALPHA-ADRENERGIC BLOCKERS

61
Q

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

A

CENTRALLY ACTING ALPHA2 AGONIST

62
Q

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

A

ADRENERGIC NEURON BLOCKERS (PERIPHERALLY ACTING SYMPATHOLYTICS)

63
Q

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)

A

ALPHA1 & BETA1 - ADRENERGIC BLOCKERS

64
Q

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

A

MACROLIDES

65
Q
  1. ERYTHROMYCIN (1950s) (Erythrocin, Erymax)
A

MACROLIDES

66
Q

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)

A

ERYTHROMYCIN (1950s) (Erythrocin, Erymax)

67
Q

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)

A

AZITHROMYCIN (ZITHROMAX)

68
Q

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)

A

CLARITHROMYCIN (KLARICID)

69
Q

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)

A

DIRITHROMYCIN (DYNABAC)

70
Q
  • 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

A

Nursing care for patients taking macrolides

71
Q

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

A

LINCOSAMIDES

72
Q

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

A

LINCOSAMIDES

73
Q

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)

A

CLINDAMYCIN (CLEOCIN)

74
Q

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)

A

LINCOMYCIN (LINCOCIN)

75
Q

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!!

A

VANCOMYCIN HCI (VANCOCIN)

76
Q

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)

A

FLUOROQUINOLONES

77
Q
  • 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

A

SULFONAMIDES

78
Q

2 CLASSIFICATIONS OF SULFONAMIDES

A
  1. SHORT ACTING
  2. INTERMEDIATE
79
Q
  1. SULFADIAZINE
  2. SULFISOXAZOLE (Gantrisin)
A

SHORT ACTING SULFONAMIDES

80
Q
  • 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)

A

SULFADIAZINE

81
Q
  • 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

A

SULFISOXAZOLE (Gantrisin)

82
Q
  1. SULFAMETHOXAZOLE (Gantanol/SMZ/SMX)
  2. SULFASALAZINE (Azulfidine)
  3. COTRIMOXAZOLE (Septa, Bactrim)
A

INTERMEDIATE ACTING SULFONAMIDES

83
Q
  • 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

A

SULFAMETHOXAZOLE (Gantanol/SMZ/SMX)

84
Q
  • 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

A

SULFASALAZINE (Azulfidine)

85
Q

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

A

COTRIMOXAZOLE (Septa, Bactrim)

86
Q
  1. CHLORAMPHENICOL (Chloromycetin)
  2. SPECTINOMYCIN HYDROCHLORIDE (Trobicin)
  3. QUINUPRISTIN / DALFOPRISTIN (Synercid)
  4. PEPTIDES
A

UNCLASSIFIED ANTIBACTERIAL DRUGS

87
Q

2 TYPES OF PEPTIDES

A

a. POLYMYXIN
b. BACITRACIN

88
Q

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

A

CHLORAMPHENICOL (Chloromycetin)

89
Q

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

A

SPECTINOMYCIN HYDROCHLORIDE (Trobicin)

90
Q
  • 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

A

QUINUPRISTIN / DALFOPRISTIN (Synercid)

91
Q

Derived from cultures of bacillus subtilis

A

PEPTIDES

92
Q
  • 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
A

POLYMYXIN

93
Q
  • 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
A

BACITRACIN