CHAPTER 42: INTRODUCTION
TO THE CARDIOVASCULAR SYSTEM
Cardiovascular System
- responsible for delivering
oxygen and nutrients to all of the cells of the body and for removing waste
products for excretion
- consists: 1. heart 2. pump3.
interconnected series of tubes
THE HEART
- hollow, muscular organ
divided into 4 chambers: atriums (
“porch” or entryway) and ventricles (
lower part)
- is the pump that keeps blood
flowing through 60,000 miles of tubes, constituting the cardiovascular system
*auricle- attached to each
atrium; collects blood that is pumped into the ventricles by arterial
contraction
** a partition called a septum
separates the right half of the heart from the left. The right receives
deoxygenated blood from everywhere in the body through the veins ( vessels that
carry blood toward the heart) and directs that blood into the lungs…
*** arteries- where aorta
delivers blood into the systemic circulation
- vessels
that carry blood away from the heart
CARDIAC CYCLE
- … each period of the
ventricles followed by a period of systole= cardiac cycle…
* myocardium
- fibers of cardiac muscle
- form two intertwining networks called atrial
and ventricular syncytia
* Starling’s law of the
heart
-occurs when muscle fibers of
the heart are stretched by the increase volume of blood that has returnedè spring back to normal size; is similar to stretching a
rubber band…
* Diastole
- the period of cardiac muscle
relaxation where the heart from the systemic and pulmonic veins, w/c flow into
the right and left…
* tricuspid- valve on the right
side of the heart; composed of 3 leaflets or cusps
mitral or bicuspid valve- valve on the left side of the heart; composed of two
leaflets or cusps
* systole
- the contraction of
ventricles
* The heart’s series of one-
way valves keeps the blood flowing on the correct direction, as follows:
1. Deoxygenated blood:
right atrium, though tricuspid valve to right ventricle, through pulmonary
valve to the lungs
2. Oxygenated blood:
through the pulmonary veins to ventricle, through aortic valve to the aorta
CONDUCTION SYSTEM OF THE HEART
- consist of:
1. SA node- located in top of
the right atrium, acts as the pacemaker of the heart
2. AV nodes- slows the
impulse, allowing for the delay needed for ventricular filling, and sends it
from the atria into the ventricles by way of the bundle of His
3. Bundle of His- w/c enters
the septum and divides into three bundle branches
4. Bundle branches- w/c
conduct impulses through the ventricles
5. Purkinje fibers- w/c
delivers the impulse the ventricular cells
***Sinoatrial (SA) node
AUTOMATICITY
- where the cells can generate
action potentials or electrical impulses without being excited to do so by
external stimuli
5 phases:
1. Phase 0- points of stimulation; where: sodium gates open along
the cell membrane, and sodium rushes into the cell, resulting in a positive
state—an electrical potentialè called depolarization
2. Phase 1- when Na ions concentrations are equal inside and
outside of the cell
3. Phase 2 (plateau stage)- cell membrane becomes less permeable to Naè Ca slowly enters the cellè K slowly leaves the cell
4. Phase 3- rapid repolarization è K rapidly moves out of the cell
5. Phase 4- cell comes to rest as the sodium- potassium pump
returns the membraneè spontaneous repolarization begins again
CONDUCTIVITY
- where the specialized cells
of the heart can conduct an impulse rapidly through the system so that the
muscle cells of the heart are stimulated at approximately the same time…
* absolute refractory period
***** SA node is the dominant
influences most of the time, keeping the resting heart rate at 70 to 80 beats
per minute
* Sarcomere- the basic unit of the cardiac muscle
- made up of two contractile
proteins: actin (thin filament) and myosin (thick filament)è kept apart by the protein troponin
* Degree of shortening- determined by the amount of Ca present—the more Ca is
present, the more bridges will be formed…
ARRYTHMIA OR DYSRYHTHMIA
- a disruption in cardiac rate
or rhythm
- interfere with the work of
the heart and can disrupt cardiac output, which affects every cell in the body
- occurs when there is a shift
in the pacemaker of the heart from the SA node to some other sit, called ectopic
focus
FIBRILLATION
- very serious arrhythmias
arise when the combination of ectopic foci and altered conduction set off an
irregular, uncoordinated twitching of the atrial or ventricular muscle
ELECTROCARDIOGRAPHY
-is a process of recording the
patterns of electrical impulses as they move through the heart
- an important diagnostic tool
in the care of the cardiac patients
ELECTROCARDIOGRAPHY MACHINE
- detects the patterns of
electrical impulse generation and conduction though the heart and translates
that information to a recorded pattern
ELECTROCARDIOGRAM
-a measure of electrical
activity; provides no information about the mechanical activity of the
heart
The normal ECG pattern is made
up of main waves:
1. P wave- formed as impulses
originating in the SA node or pacemaker pass through the atrial tissue
2. P wave- precedes the
contraction of the atria
3. Ta wave- appear around the
QRS complex
Critical points of the ECG are
as follows :
1. P-R interval: reflects the
delay of conduction at the AV node
2. Q-T interval: reflects the
critical timing of repolarization of the ventricles
3. S-T segment: reflects the
important information about the repolarization of the ventricles
TYPES OF ARRHYTHMIAS
1. Sinus arrhythmias
- has a slower- than- to
normal heart rate (usually less than 60 beats/ min) w/ Normal- appearing ECG
pattern
2. Supraventricular
Arrhythmias
- arrhythmias that originate
above the ventricles but not in the SA node
- feature an abnormally shaped
P wave
- includes the following:
a. Premature atrial
contractions (PAC’s)- reflect an ectopic focus in the atria that is generating
an impulse out of the normal rhythm
b. Paroxysmal atrial
tachycardia (PAT)- runs of rapid heart originating in the atria
c. Atrial flutter-
characterized b sawtooth- shaped P waves reflecting a single ectopic focus that
is generating a regular, fast atrial depolarization
d. Atrial fibrillation- w/
irregular P waves representing many ectopic foci firing in an uncoordinated
manner through the atria
3. Ventricular Arrhythmias
- impulses that originate
below the AV node originate from ectopic foci that do not use the normal
conduction pathways
ATRIOVENTRICULAR BLOCK
- also called heart block
- reflects a slowing or lack of conduction at
the AV node
-occur because of structural
damage, hypoxia, or injury to the heart muscle
- First degree of heart block=
P-R interval beyond the normal 0.16 to 0.20 seconds
CARDIOVASCULAR SYSTEM
CIRCULATION
- follows two courses:
1. Heart lung or pulmonary
circulation: the right side of the heart sends blood to the lungs, where carbon
dioxide and some waste products are removed from the blood and oxygen is picked
up by the red blood cells
2. Systemic circulation: the
left side of the heart sends oxygenated blood out to all of the cells in the
body
* resistance system
- also referred as arterial system
- where the vessels can either
constrict or dilate, increasing or decreasing resistance, based on the needs of
the body
* capillary system
- where blood from tiny
arterioles flows
- connects the arterial and
venous system
* capillary fluid shift
- shifting of fluid in the
capillaries
- carefully regulated between
hydrostatic (fluid pressure) forces in the arterial end of the capillary and
oncotic pressure ( the pulling pressure of the large, vascular proteins)
*Capacitance system
- also referred as venous
system
- where the veins has the
capacity to hold large quantities of fluid
* sinuses of Valsalva
- where the myocardium
receives its blood through 2 main coronary arteries that branch off the base of
the aorta
*coronary arteries
- these arteries encircle the
heart in pattern resembling a crown
*pulse pressure
- the pressure that fills the
coronary arteries
- it is systolic minus
diastolic blood pressure readings
* end- artery circulation
- a pattern of circulation
The main forces hat determine
the heart’s use of oxygen or oxygen consumption
are as follows:
1. Heart rate: the more the
heart has to pump, the more oxygen it will require to do that
2. Preload ( amount of blood
that is brought back to the heart to be pumped around): the more blood that is
returned to the heart, the harder it will have to work to pump the blood
around. The volume of blood that is determinant of preload
3. Afterload ( resistance
against which the heart has to beat): The higher the resistance in the system,
the harder the heart will have to contract to force open the valves and pump
the blood along. The blood pressure is measure of afterload
SYTEMIC ARTERIAL PRESSURE
* Hypotension
- occur if the blood pressure
falls, either from the loss of blood flowing from high- pressure to low
pressure areas
- if severe, it can progress
to shock and even death as cells are cut
off from their oxygen supply
* Hypertension
- excessive high blood
pressure
- can damage the fragile
lining of blood vessel
- cause disruption of blood
flow to the tissues
- caused by neurostimulation
of the blood vessels that cause them to constrict and to raise pressure
* Vasomotor Tone
- work to dilate the vessels
if more blood flow is needed in an area
*Cardiovascular center
- the coordination of these
impulses through the medulla
RENIN – ANGIOTENSIN SYSTEM
-determinant of Blood pressure
- activated when the blood
flow to the kidneys is decreased
-…cells in the kidney release
an enzyme called rennin
- Angiotensin I travels to
lungs è Angiotensin-
converting enzyme (ACE) è reacts è Angiotensin II = Vasoconstriction
(read: p. 635)
CONGESTIVE HEART FAILURE
- if the heart fails to do its
job of effectively pumping through the system, blood backs up and system
becomes congested
- results: hydrostatic
pressure on the venous end of the capillaries
CHAPTER 43: DRUGS AFFECTING BLOOD PRESSURE
- altering the
body’s regulatory mechanisms
- alter the normal
reflexes that control BP
- does not cure the
disease but is aimed at maintaining the BP within normal limits to prevent the
damage that hypertension can cause
Stepped-Care
Approach to Treating Hypertension
- by the Seventh
Joint National Committee on Prevention, Detection, Evaluation, and Treatment of
Hypertension, from the National Institute of Health
Step 1: Lifestyle Modifications
o weight reduction
o reduction of
sodium intake
o moderation of
alcohol intake
o smoking cessation
o increased
physical activity
Step 2: Inadequate Response
o continue
lifestyle modifications
o initial drug
selection
1. diuretic or
β-blocker
2. ACE inhibitor,
calcium channel blocker, α-blocker, α-
and β-blocker
Step 3: Inadequate Response
o increase drug
dose, or
o substitute
another drug, or
o add a second drug
from another class
Step 4: Inadequate Response
o add a second or
third agent or diuretic if not already prescribed
Diuretics
- ↑ the excretion
of sodium and water from the kidney
- first agents
tried in mild hypertension
- ↑ urination and
disturb electrolyte and acid-base balances
Sympathetic
Nervous System Blockers
- block the effects
of the SNS
- useful in
blocking many of the compensatory effects of the SNS
β-blockers
|
block
vasoconstriction; ↓ HR; ↓ muscle cardiac contraction; ↑ blood flow to
kidneys; used in monotherapy in Step 2
|
α-
and β-blockers
|
blocking
of all receptors in SNS; patients complain of fatigue, loss of libido,
inability to sleep, GI and GU disturbances
|
α-adrenergic
blockers
|
inhibit
postsynaptic α1-adrenergic receptors, ↓ sympathetic tone in the
vasculature and causing vasodilation; diagnose and manage episodes of pheochromocytoma
|
α1-blockers
|
block
postsynaptic α1-receptor sites, ↓ vasculature and causing
vasodilation; do not block presynaptic α2-receptor sites
|
α2-agonists
|
stimulate
α2-receptors in the CNS and inhibit the CV centers, ↓BP; many
adverse CNS, GI effects, cardiac dysrhythmias
|
Angiotensin-Converting
Enzyme (ACE) Inhibitors
- block the
conversion of angiotensin I to angiotension II in the lungs
- as monotherapy or
combined with diuretics
Prototype:
captopril
(Capoten)
- for hypertension,
congestive heart failure (CHF), diabetic neuropathy, left ventricular
dysfunction after MI
- associated with
fatal pancytopenia, cough, GI distress
Therapeutic
Actions and Indications
- ↓ BP and
aldosterone release
- indicated for
treatment of hypertension, alone or with other drugs
Pharmacokinetics
- well absorbed,
widely distributed
- metabolized in
liver, excreted in urine and feces
- cross the
placenta and associated with serious fetal abnormalities
Contraindications
- allergy
- impaired renal
function
- pregnancy and
lactation
Caution
- CHF
- salt/volume
depletion
Adverse
Effects
- effects of
vasodilation and alterations in blood flow
o reflex
tachycardia, chest pain, angina, CHF, cardiac arrhythmias
o GI irritation,
ulcers, constipation, liver injury
o renal
insufficiency, renal failure, proteinuria
o rash, alopecia,
dermatitis, photosensitivity
- unrelenting cough
- associated with
fetal pancytopenia and MI
Drug-Drug
Interactions
- allopurinol =
risk of hypersensitivity reactions ↑
Food-Food
Interactions
- food = absorption
of oral ACE inhibitors ↓
Nursing
Considerations
- encourage patient
to implement lifestyle changes
- administer on
empty stomach, 1 or 2 hours before meals
- monitor fluid
volume
Angiotensin II Receptor Blockers (ARBs)
- selectively bind
the angiotensin II receptors in blood vessels to prevent vasoconstriction
- prevents the
release of aldosterone in the adrenal cortex
Prototype:
losartan
(Cozaar)
- used alone or as
part of combination therapy
- treatment of
diabetic neuropathy with an elevated serum creatinine an d proteinuria
Therapeutic
Actions and Indications
- selectively bind
with angiotensin II receptor sites in vascular smooth muscle and in the adrenal
gland to block vasoconstriction and aldosterone release
- treatment of
hypertension and for CHF in patients who are intolerant to ACE inhibitors
Pharmacokinetics
- well absorbed,
metabolized in liver
- excreted in urine
and feces
- crosses the
placenta, associated with serious fetal abnormalities and death
Contraindications
- allergy
- pregnancy and
lactation
Cautions
- hepatic or renal
dysfunction
- hypovolemia
Adverse
Effects
- headache,
dizziness, syncope, weakness
- hypotension, GI
complaints
- symptoms of upper
respiratory tract infections and cough
- rash, dry skin, alopecia
Drug-Drug
Interactions
- phenobarbital =
risk of ↓ serum levels and loss of effectiveness ↑
Nursing
Considerations
- encourage patient
to implement lifestyle changes
- administer
without regard to meals; give with food
- suggest use of
barrier contraceptives
- monitor fluid
volume
Calcium Channel
Blockers
- prevent the
movement of calcium into the cardiac and smooth muscle cells
- when the cells
are stimulated
- leading to loss
of smooth muscle tone, vasodilation, ↓ peripheral resistance
- ↓ BP
- very effective
for treatment of angina
Prototype:
diltiazem
(Cardizem, Tiamate)
- sustained-release
preparation
- treatment of
hypertension
Therapeutic
Actions and Indications
- inhibit the
movement of calcium ions across the membranes of myocardial and arterial muscle
cells
Pharmacokinetics
- well absorbed,
metabolized in liver, excreted in urine
- cross the
placenta, enters breast milk
Contraindicaitons
- allergy
-
heart block or sick sinus
syndrome
- renal or hepatic
dysfunction
- pregnancy or
lactation
Adverse
Effects
- CNS effects
- GI effects
- CV effects
- skin flushing,
rash
Drug-Drun
Interactions
- cyclosporine = ↑
serum levels and toxicity of cyclosporine
Vasodilators
- produce
relaxation of the vascular smooth muscle, ↓ peripheral resistance and reducing
BP
- do not block
reflex tachycardia
- reserved for use
in severe hypertension and hypertensive emergencies
Prototype:
nitroprusside
(Nitropress)
- used
intravenously
- treatment of
hypertensive crisis and maintain controlled hypertension during surgery
- toxic levels
cause cyanide toxicity
Therapeutic
Actions and Indications
- act directly on
vascular smooth muscle to cause muscle relaxation, leading to vasodialtion and
drop in BP
Pharmacokinetics
- rapidly absorbed
and widely distributed
- metabolized in
the liver and excreted in urine
- cross the placenta
and enter breast milk
Contraindications
- allergy
- pregnancy and
lactation
- cerebral
insufficiency
Cautions
- peripheral
vascular disease, CAD, CHF, tachycardia
Adverse
Effects
- related to
changes in BP
- cyanide toxicity
may occur with nitroprusside
o dyspnea
o headache
o vomiting
o dizziness
o ataxia
o loss of
consciousness
|
o imperceptible
pulse
o absent reflexes
o dilated pupils
o pink color
o distant heart
sounds
o shallow
breathing
|
Nursing
Considerations
- monitor BP and
fluid volume
Other
Hypertensive Agents
only
drug: mecamylamine (Inversine)
- ganglionic
blocker that occupies cholinergic receptor sites of autonomic neurons, blocking
the effects of acetylcholine at both sympathetic and parasympathetic ganglia
- can cause
o severe
hypotension, CHF
o CNS symptoms of
dizziness, syncope, weakness, vision changes
o parasympathetic
blocking symptoms of dry mouth, glossitis, nausea, vomiting, constipation,
urinary retention
o impotence
ANTIHYPOTENSIVE
AGENTS
- severe
hypotension leads to shock
- sympathomimetic
drug: first choice drug for treating shock
Sympathetic
Adrenergic Agonists
- effects of a
sympathetic stress response:
o ↑ BP
o ↑ blood volume
o ↑ strength of
cardiac muscle contraction
only
drug: midodrine (ProAmatine)
- treat orthostatic
hypotension
Therapeutic
Actions and Indications
- activates
alpha-receptors in arteries and veins to ↑ in vascular tone and BP
- indicated for the
symptomatic treatment of orthostatic hypotension
Pharmacokinetics
- rapidly absorbed
in GI tract
- metabolized in
liver and excreted in urine
Contraindications
- supine hypertension,
CAD, pheochromocytoma
- acute renal
disease
- urinary retention
Cautions
- pregnancy and
lactation
- visual problems
- renal or hepatic
impairment
Adverse
Effects
- related to
stimulation of alpha-receptors
o piloerection,
chills, rash
o hypertension,
bradycardia
o dizziness, vision
changes, vertigo, headache
o problems with
urination
Drug-Drug
Interactions
- risk of ↑ effects
and toxicity of cardiac glycosides, beta-blockers, alpha-adrenergic agents,
corticosteroids if taken with midodrine
Nursing
Considerations
- monitor BP
- do not administer
to bedridden patients
- monitor HR
regularly
- monitor patients
with visual problems
- encourage
patients to void before taking drug
To download the file, click the link below
CHAPTER 44:
CARDIOTONIC AGENTS
Congestive
heart failure (CHF)
-condition where the heart fails to effectively pump
blood around the body
-
called “dropsy’ or compensation
TREATMENTS OF CHF:
1. VASODILATORS
- used to treat CHF because they can decrease the
workload of the overworked cardiac muscle
2. DIURETICS
- use to decrease blood volume, which decreases venous
return and blood pressure
- end result: decrease in afterload and preload and a
decrease in the heart’s workload
3. BETA- ADRENERGIC AGONISTS
- stimulate the beta receptors in the sympathetic
nervous system, increasing calcium flow into the myocardial cells and causing
increased contraction, positive inotropic effect
4. CARDIOTONIC DRUGS
- drugs that affect the intracellular calcium levels
in the heart muscle, leading to increased contractility
- increase in contraction strength leads to increased
cardiac output, which causes increased renal blood flow decreases rennin
release
-increases urine output
-decreased blood flow
- relieve CHF
- has two
types:
A. CARDIC
GYCOSIDES
- used for hundred of years
- derived form foxglove or digitalis plant
Drugs:
1. Digoxin (Lanoxin, Lanoxicaps)
-treatment of acute congestive heart
failure, atrial arrhythmias
* THERAPEUTIC ACTIONS
1.increase intracellular calcium and allow more
calcium to enter myocardial cells during depolarization, causing following
effects:
a. Increased force of myocardial contraction
b. Increased cardiac output and renal perfusion
c. Slowed heart rate
d. decreased conduction velocity through the
artrioventricular node
**PHARMACOKINETICS
1. absorbed widely
2. excreted unchanged in urine
3. caution w/ presence of renal impairements
4. not given during pregnancy
5. enters breast milk
*** CONTRAINDICATION
1. presence of allergy
2. tachycardia or fibrillation
3. heart block or sick sinus
syndrome
4. idiopathic hypertrophic
subaortic stenosis (IHSS)
5. acute MI
6. renal insufficiency
7. electrolyte abnormalities
****CAUTION
1. pregnant or lactating women
2. **pediatric and geriatric patients
*****ADVERSE EFFECTS
1. headache,
weakness, drowsiness and vision changes
2. GI upset and anorexia
3. risk of arrhythmia development
*****DRUG-DRUG INTERACTION
1. taken with veramil, aminodarone, quinidine,
quinine, erythromycin, tetracycline or cyclosporine = increased therapeutic
effects
NURSING CONSIDERATION
DIAGNOSIS
1. Risk for deficient fluid volume related to diuresis
2. Ineffective Tissue perfusion related in cardiac
output
3. Impaired Gas exchanged related to changes in Cadiac
Output
4. Deficient Knowledge regarding drug therapy
IMPLEMENTATION
1. Consult with the prescriber about the end for a
loading dose when beginning therapy
2. Monitor apical pulse for 1 full minute before
administration of drugs
3. Monitor pulse for any change in quality or rhythm
4. check for dosage and preparation carefully
5. Check pediatric dosage with extreme extra care
6. follow dilution instructions
7.administer IV doses very slowly at least 5 minutes
8. Avoid IM administration
9. Arrange the patient to be weighed
10. Avoid administering oral drug with food or
antacids
11. Monitor
patient digoxin level ( 0.5 to 3 ng/mL)
B.
PHOSPHODIESTERASE INHIBITORS
- belong to a second class of drugs that act as
cardiotonic (intropic) agents
Drugs:
1. Inamripone (Inocor)
- treatment of adults with congestive heart
failure not responsive to digoxin, diuretics or vasodilators
2. Milrinone (Pimacor)
- shorterm management of CHF in adults receiving
digoxin and diuretics
*THERAPEUTIC ACTIONS
1. block the enzyme phosphodiesterase
2. leads to an increase in myocardial cell cyclic
adenosine monophosphate (cAMP)
3. increases calcium levels in the cells
4. increased cellular calcium causes contraction and
prolongs effects of sympathetic stimulation
5. indicated for shortterm CHF that has not responded
to digoxin or diuretics
**PHARMACOKINETICS
1. widely
distributed after injection
2. metabolized in the liver
3. excreted in the urine
***CONTRAINDICATIONS
1. has allergy
2. w/ severe aortic or pulmonic valvular disease
3. fluid volume deficit
****CAUTIONS
1. Elderly
2. pregnant or lactating women
***** ADVERSE EFFECTS
1. ventricular
arrhythmias, hypotension and chest pain
2. GI effects: nausea, vomiting, anorexia, abdominal
pain
3. Thrombocytopenia
4. hypersensitivity reactions: vasculitis,
pericarditis, pleurititis, and ascites
*******DRUG-DRUG INTERACTION
1. avoid
Fluosemide ( Diuretics)
NURSING CONSIDERATIONS
DIAGNOSIS
1. decreased cardiac output related to arrhythmias or
hypotension
2. risk for injury related to CNS or Cardiovascular
effects
3. Innefective tissue perfusion related to hypotension
or arrythmias
4. Deficient knowledge regarding drug therapy
IMPLEMENTATION
1. Protect drug form light
2. monitor input and output
3. monitor platelet count
4. monitor injection sites
CHAPTER 45
ANTIARRHYTHMIC AGENTS
Coronary Artery Disease
(CAD)
- progressive growth of atheromatous plaques, or atheromas in the coronary
arteries
→
plaques begin as fatty streaks in the endothelium
→
they injure the endothelial lining
→
development of foam cells (by inflammatory process)
→
platelets, fibrin, other fats, and remnants collect
on the injured vessel lining
→
cause atheroma to grow
→
blood vessel narrows and limits blood flow
- injury to the vessel also causes scarring and thickening of cell wall
ü the softer, more lipid atheromas appear to be more likely to rupture
than stable, harder cores
ANTIARRHYTHMIC
DRUGS
- affect the action
potential of the cardiac cells, altering their automaticity, conductivity, or
both
- proarrhythmic:
can also produce new arrhythmias
- used in emergency
situations when the hemodynamics arising from the patient’s arrhythmia are
severe and fatal
- may block reflex
arrhythmias and help keep the CV system in balance, or they may precipitate
new, deadly arrhythmias
Class
I Antiarrhythmics
- block the sodium
channels in the cell membrane during an action potential
- local anesthetics
or membrane-stabilizing agents
- preferable in
situations such as tachycardia
Class IA Drugs
- depress Phase 0
of the action potential and prolong the duration of the action potential
o disopyramide (Norpace)
o moricizine (Ethmozine)
o procainamide (Pronestyl)
o quinidine (Quinaglute)
Class IB Drugs
- depress Phase 0
somewhat and actually shorten the duration of the action potential
o lidocaine (Xylocaine)
o mexiletine (Mexitil)
Class IC Drugs
- markedly depress
Phase 0, with a resultant extreme slowing of conduction
o flecainide (Tambocor)
o propafenone (Rythmol)
Therapeutic Actions and Indications
- binding to Na
channels, depressing Phase 0 of action potential, changing the duration of
action potential
- have a local
anesthetic effect
- treatment of
potentially life-threatening ventricular arrhythmias
Pharmacokinetics
- widely
distributed after injection of after rapid absorption through the GI tract
- undergo hepatic
metabolism
- excreted in urine
- cross the
placenta and enter breast milk
Contraindicaitons
- allergy
- bradycardia or
heart block
- CHF, hypotension,
shock
- electrolyte
disturbances
Cautions
- renal or hepatic
dysfunction
- pregnancy
Adverse Effects
- associated with
their membrane-stabilizing effects and effects on action potentials
o CNS effects
o GI effects
o CV effects
- respiratory
depression and respiratory arrest
- rash,
hypersensitivity reactions, loss of hair, bone marrow depression
Drug-Drug Interactions
- digoxin,
beta-blockers = ↑ risk for arrhythmias
- digoxin = ↑
digoxin levels and digoxin toxicity
- cimetidine = ↑
serum levels and toxicity
- oral
anticoagulants = ↑ risk for bleeding
Drug-Food Interactions
- foods that
alkalize urine (citrus juices, vegetables, antacids, milk products) = ↑
quinidine levels and toxicity
- grapefruit juice
= ↑ serum levels and toxic effects
Nursing Considerations
- monitor cardiac
rhythm
- maintain life
support equipment on standby
- give parenteral
forms only if the oral form is not feasible
- titrate the dose
to the smallest amount needed
Class
II Antiarrhythmics
- beta-adrenergic
blockers that block beta receptors, causing a depression of Phase 4 of the
action potential
- slow the recovery
of cells, leading to slowing of conduction and ↓ automaticity
Prototype: propanolol
(Inderal)
- used as an
antihypertensive, antianginal, antimigraine headache drug and as an
antiarrhythmic to treat supraventricular tachycardias caused by digoxin or
catecholamines
Therapeutic Actions and Indications
- competitively
block beta-receptor sites in the heart and kidneys
- stabilize
excitable cardiac tissue and ↓ BP
- indicated for the
treatment of supraventricular tachycardias or PVCs
Pharmacokinetics
- absorbed from GI
tract, hepatic metabolism, excreted in urine
- used only when
the benefit to the mother outweighs the risk to the fetus
Contraindications
- sinus bradycardia
(rate less than 45 beats/min) and AV block
- cardiogenic
shock, CHF, asthma, respiratory depression
- pregnancy and
lactation
Cautions
- diabetes and
thyroid dysfunction
- renal and hepatic
dysfunction
Adverse Effects
- related to the
effects of blocking beta receptors in the SNS
o CNS effects
o CV effects
o respiratory
effects
o GI effects
- loss of libido, ↓
exercise tolerance, alterations in blood glucose levels
Drug-Drug Interactions
- verapamil = ↑
risk of adverse effects
- insulin = ↑
hypoglycemia
Nursing Considerations (same as Class I Antiarrhythmics)
Class
III Antiarrhythmics
- block K channels,
prolonging Phase 3 of the action potential, which prolongs repolarization and
slows the rate and conduction of the heart
Prototype: sotalol
(Betapace, Betapace AF)
- indicated for the
treatment of documented life-threatening arrhythmias and maintenance of normal
sinus rhythm
- proarrhythmic
Therapeutic Actions and Indications
- block K channels
and slow the outward movement of K during Phase 3 of the action potential
- indicated for
o life-threatening
ventricular arrhythmias
o conversion of
recent-onset atrial fibrillation or atrial flutter to normal sinus rhythm
o maintenance of
sinus rhythm after conversion of atrial arrhythmias
Pharmacokinetics
- well absorbed and
widely distributed
- metabolized in
the liver
- excreted in the
urine
- used only when
the benefit to the mother outweighs the risk to the fetus
Cautions
- shock,
hypotension, respiratory depression, prolonged QTc interval
- renal or hepatic
disease
Adverse Effects
- related to the
changes they cause in action potentials
o nausea, vomiting,
GI distress
o weakness and
dizziness
o hypotension, CHF,
arrhythmias
- fever toxicity,
ocular abnormalities, serious cardiac arrhythmias
Drug-Drug Interactions
- digoxin or
quinidne = serious toxic effects
Class
IV Antiarrhythmias
- block Ca channels
in the cell membrane, leading to depression of depolarization and a
prolongation of Phases 1 and 2 of repolarization, slowing automaticity and
conduction
Prototype: diltiazem
(Cardizem)
- administered IV
- treat paroxysmal
supraventricular tachycardia
Therapeutic Actions and Indications
- block the
movement of Ca ions across the cell membrane, depressing the generation of
action potentials, delaying Phases 1 and 2 or repolarization, and slowing
conduction through the AV node.
- treatment of
supraventricular tachycardia and to control the ventricular response to rapid
atrial rates
Pharmacokinetics
- well absorbed
- metabolized in
liver and excreted in the urine
- used only when
the benefit to the mother outweighs the risk to the fetus
Contrindications
- allergy
- sick sinus
syndrome or heart block
- lactation
- CHF or hypotension
Caution
- idiopathic
hypertrophic subaortic stenosis (IHSS)
- impaired renal or
liver function
Adverse Effects
- related to their
vasodilation of blood cells throughout the body
o CNS effects
o GI effects
- hypotension, CHF,
shock, arrhythmias, edema
Drug-Drug Interactions
- beta-blockers = ↑
risk of cardiac depression
- digoxin =
additive AV slowing
- dogixin,
carbamazepine, prazosin, quinidine = ↑ serum levels and toxicity
-
atracurium, gallamine,
metocurine, pancuronium, rocuronium, tubocurarine, vecuronium = ↑ respiratory
depression
- calcium products
or rifampin = ↓ effects
- given IV within
48 hours if IV beta-adrenergic drugs = risk of severe cardiac effects
- diltiazem +
cyclosporine = ↑ serum levels and toxicity
Nursing Considerations (same as Class I Antiarrhythmics)
Other
Drugs Used to Treat Arrhythmias
adenosine (Adenocard)
- convert
supraventricular tachycardia to sinus rhythm
- drug of choice
for terminating supraventricular tachycardia
o very short
duration of action (15 sec), picked up by circulating RBCs, and cleared through
the lvier
o associated with
very few adverse effects
digoxin (Lanoxin, Lanoxicaps)
- slows Ca from
leaving cell, prolonging the action potential and slowing conduction and HR
- treatment for
atrial arrhythmias
- positively
inotropic, leading to ↑ cardiac output
Nursing Considerations (same as Class I Antiarrhythmics)
CHAPTER 46: ANTIANGINAL
AGENTS
ANTIANGINAL DRUGS
-
are used to help restore the supply- and- demand ratio in oxygen delivery to
the myocardium when rest is not enough
-
these drugs can work to improve blood delivery to the heart muscle in 2 ways:
1.
by dilating blood vessels ( e.i. increasing the supply of oxygen)
2.
by decreasing the work of the heart (i.e. decreasing the demand of oxygen)
I. Nitrates
-
are drugs that act directly on smooth muscle to cause relaxation and to depress
muscle tone
-
decreases: preload, afterload, myocardial contractility , oxygen demand
Prototype: Nitrogylcerin (Nitro-Bid, Nitrostat)
- treatment of acute angina attack; prevention of anginal attacks
Therapeutic
Actions and Indications
-
direct relaxation of smooth muscle with a resultant decrease in venous return
and decrease in arterial pressure, effects that reduce cardiac workload and
decrease myocardial oxygen consumption
Pharmacokinetics
1.
rapidly absorbed
2.
metabolized in liver
3.
excreted in urine
4.
cross placenta
5.
enter breast milk
Contraindications:
1.
presence of allergy
2.
w/ severe anemia
3.
w/ head trauma or cerebral hemorrhage
4.
during pregnancy and lactation
Caution
1.
patients with hepatic or renal disease
2.
w/ hypotension, hypovolemia, and conditions that limit cardiac output
Adverse
Effects
1.
CNS effects: headache, dizziness, weakness
2.
GI effects: nausea, vomiting, incontinence
3.
cardiovascular problems: hypotension, reflex tachycardia, syncope, angina
4.
skin related effects: flushing, pallor, increased perspiration
5.
dermatitis and local hypersensitivity reactions
Dug-
drug interaction
- ergot derivatives=
risk of hypertension and decreased anti- anginal effects
- heparin = decreased
effects
Nursing
Considerations:
1.
Give SQ preparations in the tongue or in buccal pouch, and encourage the
patient not to swallow
2.
ask the patient if the tablet “ fizzles” or burns
3.
Give sustained- release forms with water and caution the patient not patient
not to chew or crush them
4.
Rotate the sites of topical forms
5.
Make sure that transligual spray is used to under the tongue and not inhaled
6.
Break an amyl nitrate capsule and wave it under the nose of the angina patient
7.
Taper the dosage gradually
II. Beta- Blockers
-
used to block the stimulatory effects of the sympathetic nervous system
-
block beta- adrenergic receptors and vasoconstriction
-
prevent the increase in heart rate and increased intensity of myocardial
contractility that occur with sympathetic stimulation such as exertion or
stress
-
decrease the cardiac workload
Prototype: metoprolol
(Toprol, Toprol XL)
- treatment of stable angina pectoris and hypertension; prevention
of reinfarction in MI patients, and treatment of stable, symptomatic CHF
Therapeutic
Actions and Indications
1.
completely block- adrenergic receptors in the heart and juxtaglomerular
apparatus, decreasing the influence of the sympathetic nervous system on these
tissues and thereby decreasing the excitability of the heart, decreasing
cardiac output, decreasing cardiac oxygen compensation and lowering blood
pressure
Pharmacokinetics
1.
absorbed from the GI tract and undergo hepatic metabolic
2.
found to increase bioavailability of propranolol, but this effect has not been
found with other beta- adrenergic blocking agents
3.
excreted in the urine
4.
has teratogenic effects
Contraindications:
1.
w/ bradycardia, heart block, cardiogenic shock, asthma, or COPD
2.
pregnancy and lactation
Caution:
1.
with diabetes, peripheral vascular disease or thyrotoxicosis
Adverse
Effects
1.
CNS effects: dizziness, fatigue, emotional depression and sleep disturbances
2.
GI problems: gastric pain, nausea, vomiting , colitis and diarrhea
3.
Cardiovascular effects: congestive heart failure, reduced cardiac output, and
arrhythmias
4.
Respiratory symptoms: bronchospasm, dyspnea, and cough
Drug- Drug interaction
1. beta blockers= paradoxical hypertension
2.
w/ clonidine= withdrawal
NURSING
CONSIDERATIONS ( same with beta blockers : Chapter 31)
III. CALCIUM CHANNEL
BLOCKERS
-prevent
the movement of calcium into the cardiac and smooth muscle cells when the cells
are stimulated, interfering with their ability to contract
Prototype: diltiazem
( Cardizem, Cardizem SR)
- treament of prinzmetal’s angina, effort- associated angina,
chronic stable angina; used to treat essential hypertension, paroxysmal
supraventricular tachycardia
Therapeutic
Actions and Indications
·
inhibit the
movement of calcium ions across the membranes of myocardial and arterial muscle
cells, altering the action potential and blocking muscle cell contraction
Pharmacokinetics
1. well absorbed
2.
metabolized in the live
3.
excreted in urine
4.
cross placenta and enter milk
5.
fetal toxicity reported
Contraindications
1.
presence of allergy
2.
with heart block or sick sinus syndrome
3.
with renal or hepatic dysfunction
4.
during pregnancy and lactation
Adverse
Effects
1.
CNS effects: dizziness, light- headedness, headache, fatigue
2.
GI effects: nausea and hepatic injury
3.
Cardiovascular effects: hypotension, bradycardia, peripheral edema, and heart
block
4.
Skin effects: flushing and rash
Drug-Drug
interactions
1.
toxicity of cyclosporines if taken w/ diltiazem
2.
increased risk of heart block and digoxin toxicity if combined with verapamil
NURSING
CONSIDERATIONS
1.monitor
patient’s blood pressure, cardiac rhythm, cardiac output while the drug is
titrated or dosage is being changed
2.
Monitor blood pressure very carefully if the patient is also taking nitrates
3.
Periodically monitor blood pressure and cardiac rhythm while the patient is
using these drugs
CHAPTER 47
LIPID-LOWERING AGENTS
Coronary Artery Disease (CAD)
- progressive growth of
atheromatous plaques, or atheromas in the coronary arteries
→
plaques
begin as fatty streaks in the endothelium
→
they
injure the endothelial lining
→
development
of foam cells (by inflammatory process)
→
platelets,
fibrin, other fats, and remnants collect on the injured vessel lining
→
cause
atheroma to grow
→
blood
vessel narrows and limits blood flow
- injury to the vessel
also causes scarring and thickening of cell wall
ü the softer, more lipid
atheromas appear to be more likely to rupture than stable, harder cores
ANTIHYPERLIPIDEMIC
AGENTS
- often used in
combination
- should be part of an
overall health care regimen that includes exercise, dietary restrictions, and
lifestyle changes to ↓ risk of CAD
Bile Acid
Sequestrants
Prototype: cholestyramine (Questran)
- powder mixed with
liquids and taken up to 6 times a day
Therapeutic Actions
→
bind
with bile acids in the intestine to form a complex that is excreted in the
feces
→
liver
must use cholesterol to make more bile acids
→
↓
serum levels of cholesterol and LDLs
Indications
- reduce serum cholesterol
in patients with primary hypercholesterolemia as an adjunct to diet and
exercise
- cholestyramine: treat
pruritus associated with partial biliary obstruction
Pharmacokinetics
- form an insoluble
complex
- excreted in feces
- not absorbed
systematically
Contraindications
- allergy
- complete biliary
obstruction
- abnormal intestinal
function
- pregnancy or lactation
Adverse Effects
- direct GI irritation
- ↑ bleeding times
- vitamin A and D
deficiencies
- muscle aches and pains
Drug-Drug Interactions
- ↓ or delay the
absorption of thiazide diuretics, digoxin, warfarin, thyroid hormones,
corticostreriods:
Nursing Considerations
- do not administer
powdered agents in dry form (mix with juices, soups, etc.)
- ensure tablets are not
cut, chewed, or crushed
- give drug before meals
- administer oral
medicatiosn 1 hour before or 5 to 6 hours after the bile acid sequestrant
- arrange for bowel
program
HMG-CoA
REDUCTASE INHIBITORS (“statins”)
Prototype: atorvastatin (Lipitor)
- associated with severe
liver complications
Therapeutic Actions
→
block
the formation of cellular cholesterol
→
↓
serum cholesterol and LDLs, slight ↑ or no change in HDLs
Indications
- adjuncts with diet and
exercise for the treatment of ↑ cholesterol and LDL levels
- slow the progression of
CAD
- prevent first MI
Pharmacokinetics
- absorbed from GI tract
- first-pass metabolism in
liver
- excreted through feces
and urine
- pregnancy category X
Contraindications
- allergy
- active liver disease or
history of alcoholic liver disease
- pregnancy or lactation
Caution
- impaired endocrine
function
Adverse Effects
- GI system
- CNS effects
- ↑ concentration of liver
enzymes
- rhabdomyolysis with
acute renal failure
Drug-Drug Interactions
- erythromycin,
cyclosporine, gemfibrozil, niacin, antifungal drugs = ↑ risk for rhabdomyolysis
- digoxin, warfarin = ↑
serum levels and resultant toxicity
- oral contraceptives = ↑
estrogen levels
- grapefruit juice = ↑
serum levels and risk of toxicity
Nursing Considerations
- administer drug at
bedtime
- monitor serum
cholesterol and LDL levels, including liver function, before and during therapy
- arrange for ophthalmic medications
- ensure patient has
attempted a cholesterol-lowering diet and exercise program for at least 3 to 6
months before therapy
- encourage patient to
make lifestyle changes
Cholesterol
Absorption Inhibitors
Prototype: ezetimibe (Zetia)
Therapeutic Actions
→
works
in the brush border of the small intestine to ↓ absorption of dietary
cholesterol
→
drop
in serum cholesterol levels
Indications
- lower cholesterol level
- treatment for homozygous
familial hypercholesterolemia
- reduce elevated
sitosterol and campesterol levels
Pharmacokinetics
- absorbed well
- metabolized in the liver
and small intestine
- excretion is through
feces an urine
Contraindications
- allergy
- pregnancy, lactation,
severe liver disease (if in combination with statin)
Cautions
- pregnancy or lactation
- elderly patients or with
liver disease
Adverse Effects
- mild abdominal pain and
diarrhea
- headache, dizziness,
fatigue, upper respiratory tract infection (URI), back pain, muscle aches and
pains
Drug-Drug Interations
- cholestyramine,
fenofibrate, gemfibrozil, antacids = ↑ risk of elevated serum levels of
ezetimibe
- cyclosporine = ↑ risk of
toxicity
- fibrate = ↑ risk of
cholethiasis
- ezetimibe = ↑ warfarin
levels
Nursing Considerations
- monitor serum
cholesterol, triglyceride, LDL levels, liver function test before and during
therapy
- ensure patient has
attempted a cholesterol-lowering diet and exercise program for several months
before therapy
- encourage patient to
make lifestyle changes
Other
Drugs Used to Affect Lipid Levels
fibrates
→
stimulate
the breakdown of lipoproteins from the tissues and their removal from the
plasma
→
↓
in lipoprotein and triglyceride synthesis and secretion
- absorbed from GI tract
- metabolized in liver
- excreted in urine
vitamin B3
→
inhibits
release of free fatty acids from adipose tissue
→
↑
rate of triglyceride removal from plasma
→
↓LDL
and triglyceride level, ↑ HDL levels
→
also
↓ levels of apoproteins needed to form chylomicrons
- associated with intense
cutaneous flushing, nausea, abdominal pain, development of gout
- given at bedtime
- administer 4 to 6 hours
after the bile acid sequestrant
Combination
Therapy
- if the patient shows no
response to strict dietary modifications, exercise, and lifestyle changes, and
the use of lipid-lowering agent, combination of therapy may be initiated to
achieve desirable serum LDL and cholesterol levels
CHAPTER 48 – Drugs Affecting Blood Coagulation
CARDIOVASCULAR SYSTEM
-
is a closed system
·
Consistently, the
system must maintain an intricate balance between the tendency to clot or form
a solid state, called coagulation,
and the need to “unclot” or reverse coagulation to keep the vessel open and the
blood flowing…
·
Blood coagulation
- is a complex process that
involves vasoconstriction, platelet clumping or aggregation, and a cascade of
clotting factors produced by the liver that eventually react to break down
fibrinogen ( a protein also produced in the liver) into soluble fibrin threads
.
·
Vasoconstriction
- can seal off any break and
allow the area to heal
·
Platelet
aggregation
- causes platelets in the circulating
blood to stick or adhere to the site of injury èplatelets release ADP (adenosine triphosphate-
precursor of prostaglandin) and other chemicals that attract other platelets,
causing them to gather or aggregate and to stick as wellè thromboxane A2 cause local vasoconstriction = platelet
aggregation and adhesion
·
Hageman Factor
ANTICOAGULANTS
- are drugs that interfere
with the normal coagulation process
- affect the process at any
step to slow or prevent clot formation
I. ANTIPLATELET DRUGS
- alter the formation of the
platelet plug, or
- decrease the formation of
the platelet plug by decreasing the responsiveness of the platelet to stimuli
that would cause them to stick and aggregate a vessel wall
- effectively to treat
cardiovascular diseases that are prone to produce occluded vessels; for the
maintenance of venous and arterial grafts; to prevent cerobrovascular
occlusion, and adjuncts to thrombolytic therapy in the treatment of MI and
prevention of infarction
Prototype: Aspirin ( generic)
- reduction of the risk if
recurrent TIAs or strokes in males with history of TIA due to fibrin or
platelet emboli; reduction of death or nonfatal MI patients with history of
infarction or stable angina; MI prophylaxis, also used as anti-inflammatory,
analgesics, and anti-pyretic
Therapeutic Actions:
·
inhibit platelet
adhesion and aggregation by blocking receptor sites on the platelet membrane,
preventing platelet- platelet interaction of the interaction of platelets w/
other clotting chemicals
Pharmacokinetics
·
well absorbed
·
highly bound to
plasma proteins
·
metabolized in the
liver
·
excreted in urine
·
increased bleeding
Contraindications
1. presence of allergy
2. during pregnancy and
lactation
Caution
1. Presence of Known bleeding
disorder
2. recent surgery
3. closed head surgeries
Adverse Effects
1. Bleeding ( increased
bruising and bleeding while bruising the teeth)
2. Headache, dizziness, and
weakness
3. Nausea and GI distress may
occur
4. Skin rash
Drug- Drug interactions
·
risk of excessive
bleeding increases if any of these drug is combined with another drug that
affects blood clotting
Nursing considerations
1. provide small and frequent
meals
2. provide comfort measures
and analgesia for headache
3. suggest safety measures,
including the use of electric razor and avoidance of contact sports
4. provide increase
precautions against bleeding
5. Mark the chart of any
patient teaching receiving this drug
6. Provide thorough patient
teaching, including the name of the drug, prescribed, measures to avoid adverse
effects, warning signs of problems, the need for periodic monitoring and
evaluation
II.
ANTICOAGULANTS
Interfere with coagulation
process by interfering with the clotting cascade and thrombin formation
Therapeutic Actions and Indications
Anticoagulants interfere with
the normal cascade of events involved in the clotting process. Warfarin causes
a decrease in the production of vit. K—dependent clotting factors in the liver.
Heparin, argatroban and bivalirudin block while Antithrombin formationof
thrombinfrom prothrombin. These drugs are used to treat thromboembolic
disorders such as atrial fibrillation, MI, pulmonary embolus, and evolving
dtroke and to prevent the formation of thrombi.
Prototype: Heparin (generic) half-life 30-180 minutes, metabolize in the cells and
excreted in the urine
SQ onset 20-6- minutes, peak 2-4 hours,
duration 8-12 hours
IV – immediate onset, peak
minute, duration 2-6 hours
Warfarin – effects last 4-5
days, onset of action in 3 days
Contraindications
Contraindicated to known
allergy to the drugs. They should not be use with conditions that can increase
bleeding tendencies; hemorrhagic disorders, recent trauma, spinal puncture, GI
ulcers, recent surgery, intraunterine device placement, tuberculosis, presence
of indwelling catheter, and threatened abortion.Contratindicated to pregnancy,
lactation, renal or hepatic disease
Cautions
In patients with CHF,
thyrotoxicocic, saenility, or psychosis, diarrhea, fever
Adverse effects
The most common adverse effect
is bleeding (bleeding in gums with tooth brushing to severe intrernal
hemorrhage), clotting shoud be monitored. Nausea, GI upset, diarrhea, and
hepatic dysfunctiondue to toxicity. Warfarin can cause alopecia,dermatitis,
bone marrow depression and prolonged and painful
erections.
Drug to drug Interaction
Heparin + (oral
anticoagulants, salicylates, penicillins, cephalosporins) =Increase bleeding
Heparin + nitroglycerin =
Decrease coagulation
Nursing Considerations
-screen for allergy
-evaluate for therapeutic effects
of warfarin --prothrombin time (PT) 1.5 to 2.5 times control value or ratio of
PT to INR (International Normalized Ratio) of 2 to 3
-Evaluate for herapeutic
effects of heparin—whole blood clotting time (WBCT) 2.5 to 3 times control
or activated partial thromboplastin
time (APTT) 1.5 to 3 times the control value
- evaluate for signs of blood
loss
-maintain antidotes on standby
(protamine sulfate for heparin, vit, K for warfarin)
-monitor the patient when a
drug is added or withdrawn from the drug regimen of a patient receiving warfarin
-make sure patient receives
regular follow up and monitoring
-provide health teaching, name
of drug and its effects
Low Molecular-Weight Heparins
These drugs inhibit thrombus
and clot formation by blocking factors Xa and IIa. Because of size and nature
of their molecules, theses drugs do not greatly affect thrombin, clotting or
PT; they cause fewer adverse effects. They block angiogenesis, process that
allows cancer cells to develop new blood
vessels.
Prototype: Strptokinase (streptase, kabikinase)
Therapeutic actions and indications
Thrombolytic agents work to
activate the natural clotting system, conversion of plasminogen to plasmin,
which in turn breaks down fibrin threads in a clot to dissolve a formed clot.
They are indicated for the treatment of MI, to treat pulmonary emboli and
ischemic stroke and to open clotted IV catheter.
Pharmacokenetics
Must me injected and cleared
from the body after liver metabolism, crosses the placenta and have adverse
fetal effects, should not be used during pregnancies unless benefits to the
mother out ways the potential risks to the fetus. Cautions should be used
during lactation.
Contraindications and cautions
Contraindicated to allergy of
these drugs, should not be used with conditions that could worsen the
dissolution of clots, recent surgery, active internal bleeding, cerebrovascular
accident within the last two months, aneurysm, recent serious GI bleeding,
liver disease.
Adverse effects
The most common adverse effect
is bleeding, cardiac arrhythmias and hypotensions
Drug to drug interaction
Risk of hemorrhage increases
if thrombolytic agents are used with anticoagulant or antiplatelet drug.
Nursing consideration
-Discontinue heparin if given
before administration of thrombolytic agent, unless ordered for coronary artery
infusion.
-evaluate for signs of blood
loss (bleeding gums, bruises, dark colored stools and urine, petechiae)
-institute treatment within 6
hours after the onset of symptoms of acute MI
-arrange to type and cross
match blood.
-monitor cardiac rhythm
-increase precautions against
bleeding during invasive procedures.
Drugs used to control bleeding
On the other end of the
spectrum of coagulation problems are various bleeding disorders: hemophilia, a
genetic lack of clotting factor that leaves the patient vulnerable to excessive
bleeding with injury.
Liver disease, clotting
factors and proteins needed for clotting are not produce.
Bone marrow disorders,
insufficient platelets are formed.
Antihemophilic agents
Drugs used to treat hemophilia
are replacement factors for the specific clotting factors that are genetically
missing.
Prototype: Antihemophilic factor (bioclate, others)
Therapeutic actions and indications
Replace clotting factors that
are either genetically missing or low in a particular type of hemophilia. Used
to prevent blood loss from injury or surgery and treat bleeding episode.
Pharmacokenetics
Replace normal clotting
factors and are processed as such by the body.
Contraindications and cautions
Contraindicated in the
presence of known allergy to mouse proteins. Factor IX is contraindicated in
the presence of liver disease with signs of Intravascular coagulation or
fibrinolysis. Coagulation factor VII is contraindicated with known allergies to
mouse, hamster or bovine products. Not recommended during lactation and
pregnancy.
Adverse effects
The most common is risks with
the use of blood products, e.g. hepatitis, aids. Headache, flushing, chills,
fever and lethargy. Nausea, vomiting and itching, stinging and burning at
injection site
Nursing consideration
-administer by IV only
-monitor clinical response and
clotting factor levels regularly.
-monitor for sign of
thrombosis
-decrease the rate of infusion
if headache, chills, fever or tingling occurs.
-arrange to type and cross
match blood.
Systemic hemostatic agents
A used to stop bleeding. Some
situation result in fibrinolytic state with excessive plasminogen activity and
risk of bleeding from clot dissolution.
Prototype: Aminocaproic acid (amicar)
Pharmacokinetics
Parameters are different for
each drug
Therapeutic actions and indications
Stop the natural plasminogen
clot – dissolving mechanism by blocking its activation or by directly
inhibiting plasmin. These drugs are used to prevent or treat excess bleeding in
hyperfibrinolytic states, including repeat CABG surgery.
Contraindications and cautions
Contraindicated to allergy to
these drugs and with acute DIC. Caution should be used in the following
conditions: cardiac disease, renal and hepatic dysfunction, pregnancy and
lactation
Adverse effects
The most common is excessive
clotting. CNS effects include hallucinations, drowsiness, dizziness, headache
and psychotic states. GI effects including nausea, cramps, and diarrhea.
Drug to drug interaction
Increase risk of bleeding if
combined with heparin
Nursing considerations
-monitor clinical response and
clotting factor levels
-monitor for signs of
thrombosis
-orient patients and offer
support and safety measure if hallucinations or psychoses occur.
Topical hemostatic agents
Used to injuries that involve
damage to the small vessels in the area that clotting does not occur and blood
is slowly and continually lost
Absorbable gelatin (gellfoam)
and microfibrilar collagen (avitene), are apllied directly to the injured area
until the bleeding stops
Thrombin (thrombinar,
thrombostat) derived from bovine sources and mixed with the blood
CHAPTER 49: DRUGS USED TO TREAT ANEMIAS
BLOOD
- essential for cell
survival
o contains oxygen and nutrients and removes waste products that could be toxic to
the tissues
o contains clotting factors that help maintain the vascular system
and keep it sealed
o contains important components of the immune system that protect the body
from infection
Blood
Components
- composed of liquid and
formed elements: plasma, leukocytes, erythrocytes, platelets
Types of
Anemia
1. Deficiency Anemia
- occurs when the diet
cannot supply enough of a nutrient, or enough of a nutrient cannot be absorbed
2. Megaloblastic Anemia
- occurs when the bone
marrow contains a large number of megaloblasts, or large, immature RBCs
- because these RBCs are
so large, they become crowded in the bone marrow and fewer RBCs are produced
- patients usually have a
lack of vitamin B12 or folic acid
Iron
Deficiency Anemias
- a negative iron balance
- occurs in situations in
which blood is being lost (such as heavy menstrual flow, internal bleeding)
- only enough iron is
absorbed to replace the amount of iron lost each day
- only about 1 mg of iron
is lost every day
Megaloblastic
Anemias
- there is no sufficient
folic acid or vitamin B12 to adequately create the stromal structure
needed in a healthy RBC
Folic Acid Deficiency
- folic acid is essential
for cell division in all types of tissue
- deficiencies in folic
acid are first noticed in rapidly growing cells
- may occur in:
o certain malabsorption
states (such as sprue or celiac diseases)
o malnutrition that
accompanies alcoholism
o repeated pregnancies
o extended treatment with
certain antiepileptic medications
- treated by the
administration of folic acid or folate
Vitamin B12 Deficiency
- vitamin B12
is used in minute amounts by the body and is stored for use
- it is necessary for the
health of the RBCs and for the formation and maintenance of the myelin sheath
in the CNS
- vitamin B12
deficiency may occur in:
o strict vegetarians
o inability of the GI
tract to absorb the needed amounts of vitamin B12
- treated with vitamin B12
replacement therapy
Pernicious Anemia
- occurs when the gastric
mucosa cannot produce intrinsic factor and vitamin B12 cannot be absorbed
- person may complain of
fatigue, lethargy, and CNS effects because of damage to the myelin sheath
- treated with injections
of vitamin B12 to replace the amount
ERYTHROPOIETINS
- for patients who are no
longer able to produce erythropoietin in the kidneys
Prototype: epoetin alfa
(Epogen, Procrit)
Therapeutic Actions
- acts like the natural
glycoprotein erythropoietin to stimulate the production of RBCs in the bone
marrow
Indications
- treatment of anemia with
renal failure
- to ↓ the need for blood
transfusion in patients undergoing surgery
- treatment of anemias
related to treatment for AIDS
- treatment of anemia
associated with cancer chemotherapy (Procrit
only)
Pharmacokinetics
- metabolized through the
normal kinetic process
- half life of 4 to 13
hours
Contraindications
- presence of uncontrolled
hypertension
- allergy
- lactation
Adverse Effects
- result of cellular
response to glycoprotein: CNS effects
- nausea, vomiting,
diarrhea
- related to ↑ in RBC
numbers: CV symptoms
Nursing Considerations
- confirm chronic, renal
failure before drug administration
- give epoetin alfa 3
times a week, IV or SQ
- do not mix with any
other drug solution
- monitor access lines for
clotting
- arrange for hematocrit
reading before drug administration
- evaluate iron stores
before and during therapy
- maintain seizure
precautions on standy
IRON
PREPARATIONS
- iron deficiency anemia
is common in certain groups:
o menstruating women
o pregnant and nursing
women
o rapidly growing
adolescents
o persons with GI bleeding
and slow bleeding
Prototype: ferrous sulfate (Feosol)
Therapeutic Actions
- elevate the serum iron
concentration
Indications
- treatment of iron
deficiency anemias
- adjunctive therapy in
patients receiving epoetin alfa
Pharmacokinetics
- absorbed from small
intestine
- transported in the blood
- used during pregnancy
and lactation
Contraindications
- allergy
- hemochromatosis
(excessive iron)
- hemolytic anemias
- normal iron balance
- peptic ulcer, colitis,
regional enteritis
Adverse Effects
- direct GI irritation
- with increasing serum
levels, iron can be CNS toxic, causing coma and death
- parenteral iron: severe
anaphylactic reactions, local irritation, staining of the tissues, phlebitis
Drug-Drug Interactions
- antacids, tetracyclines,
cimetidine = ↓ iron absorption
- ciproflaxin, norfloxacin,
ofloxacin = ↓ anti-infective response
- chloramphenicol = ↑ iron
levels
- levodopa = ↓ effects of
levodopa
Drug-Food Interactions
- antacids, eggs, milk,
coffee, tea = iron is not absorbed
Nursing Considerations
- confirm deficiency
anemia before drug administration
- administer with meals
- have patients drink
solutions through a straw
- caution patient that
stool may be dark or green
- administer IM only
through Z-track technique
- arrange for hematocrit
and hemoglobin measurements before and during therapy
FOLIC ACID
DERIVATIVES AND VITAMIN B12
Folate deficiencies usually occur
o secondary to ↑ demands
o absorption problems in
the small intestine
o secondary to the
malnutrition of alcoholism
Prototype: folic acid (Folvite)
- parenteral drugs are
preferred for patients with potential absorption problems
Vitamin B12 deficiencies usually
occur
o with poor diet or
increased demand
o lack of intrinsic factor
in the stomach
Prototype: hydroxocobalamin
(Hydro-Crysti 12)
- given IM everyday for 5
to 10 days, then once a month for life
- used in states of ↑
demand or dietary deficiency
Therapeutic Actions
- folic acid and vitamin B12
: for cell growth and division, and production of strong stroma in RBCs
- Vitamin B12:
maintenance of the myelin sheath in nerve tissue
Indications
- replacement therapy for
dietary deficiencies
- replacement in
high-demand states (such as pregnancy and lactation)
- treat megaloblastic
anemia
- folic acid: rescue drug
for cells exposed to some toxic chemotherapeutic agents
Pharmacokinetics
- well absorbed after
injection
- metabolized mainly in
liver
- excreted in urine
- highly protein bound
- considered essential
during pregnancy and lactation
Contraindication
- allergy
Cautions
- pregnant or lactating
who have anemias
- nasal cyanocobalamin
- presence of nasal
erosion or ulcers
Adverse Effects
- pain and discomfort at
injection sites
- nasal irritation with
the use of nasal sprays
Nursing Considerations
- confirm the nature of
megaloblastic anemia
- give both types of drugs
in pernicious anemia
- parenteral Vitamin B12
must be given IM each day for 5 to 10 days, then once a month for life
- arrange for nutritional
consultation
- monitor for
hypersensitivity reactions
- arrange for hematocrit
and hemoglobin measurements before and during therapy
Chapter 50 -
Introduction to the Kidneys and the Urinary Tract
Renal system:
- Urinary
tract
- Ureters
- Urinary
bladder
- Urethra
4 major functions of the renal system:
- Maintain
the value and composition of the body fluids w/in normal range
- Regulating
vitamin D activation
- Regulating
blood pressure
- Regulating
red blood cell production
>the kidneys are two small organs that receive about 25% of the cardiac output
Nephron
- the
functional unit of the kidneys
- is
composed of the Bowman’s capsule, proximal convoluted tubule, loop of Henle, distal convoluted tubule, and
collecting duct
Renal Processes
a.) Filtration - straining fluid into the
nephron
>approximately 125 mL of fluid
is filtered each minute, or 180L/day
>99% of the filtered fluid is
returned to the bloodstream
>approx. 1% of the filtrate,
less than 2 L of fluid is excreted each day in the form of urine
b.) Secretion – actively removing
components from the capillary system and depositing them into the tubule
c.) Absorption – removing from the tubule
to return them to the capillary system and circulation
>about 99% of the water filtered at the glomerulus is reabsorbed
>the filtrate
components include the vitamins, glucose, electrolytes, sodium bicarbonate, and
sodium chloride
>precision of the reabsorption process allows the body to
maintain the correct extracellular fluid volume and composition
Maintenance of Volume and composition of Body Fluids
Sodium Regulation
Sodium
Ø Is
one the body’s major cations(positively charged ions)
Ø Reabsorbed
via transport system that functions under the influence if the catalyst carbonic anhydrase, à carbonic acid à sodium bicarbonate
2 hormones that influence sodium levels in the filtrate:
Ø Aldosterone-a
hormone produced the adrenal gland
-
is released into the circulation in response to the
high potassium levels, sympathetic stimulation, or angiotensin III
-
stimulates Na-K exchange pump in the cells of the
distal tubule, w/c reabsorbs Na in exchange for K, as a result Na is reabsorbed
into the system and K lost in the filtrate
Ø Natriuretic
Hormone- probably produced by the
hypothalamus
-
causes decrease in Na reabsorption from the distal
tubules w/ a resultant dilute urine or increase volume
-
is released in response to the fluid overload or
hemodilution
Countercurrent
Mechanism
Ø in
the medullary nephrons allow for the concentration or dilution of urine under
the influence of ADH secreted by the hypothalamus
Potassium Regulation
Potassium
Ø is
another cation that ios vital to proper functioning of the nervous system,
muscles, and cell membranes
Ø 65%
is filtrated at the glumerulus is reabsorbed at the Bowman’s capsule and
proximal convoluted tubule
Ø 25%-30%
is r5eabsorbed at the loop of Henle
Chloride Regulation
Chloride
Ø Is
an important negatively charged ion that helps to maintain electrical
neutrality with the movement of cations across the cell membrane
Ø Primarily
absorbed in the loop of Henle, where it promotes the movement of sodium out of
the cell
*the kidneys play a role
Sodium Regulation
Calcium
ü Is
important in muscle function, blood clotting, bone formation, contraction of
cell membranes and muscle movement.
ü Filtered
at the glomerulus and mostly reabsorbed in the proximal convoluted tubule and
ascending Loop of Henle.
ü Fine
tuning reabsorption occurs in the distal convoluted tubule.
Urinary Tract
Urinary Bladder- is the
muscular pouch that stretches and holds the urine until it is excreted from the
body.
Uterus- have
smooth endothelial lining and circular muscular linings.
- The
female urethra is very short and leads to an area populated by normal
flora including e.coli.
- The
male urethra is much longer and passes through the prostate gland.
Prostate
Gland- a small gland that produces an acidic fluid that is important in
maintaining the sperm and lubricating the tract.
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CHAPTER 51: Diuretic Agents
Diuretic Agents
-
drugs that
increase the amount of urine
-
the greater
significance of diuretics is their ability to increase sodium excretion.
Therapeutic actions and indications:
-
prevent the cell’s
lining the renal tubule from reabsorbing an excessive proportion of the sodium
ions in the glomerular filtrate.
-
as a result,
sodium and other ions are lost in the urine instead of being return to the
blood, where they would cause increase intravascular volume and therefore
increase hydrostatic pressure, which could result in leaking of fluids at the
capillary level.
-
Indicated for the
treatment of edema associated with congestive heart failure, acute pulmonary edema, liver disease, and
renal disease, and for the treatment of hypertension.
-
Also use to
decrease fluid pressure in the eye (intraocular pressure), which is useful in
treating glaucoma.
-
Diuretics that
decrease potassium levels may also be indicated in the treatment of conditions
that cause hyperkalemia.
Contraindications and cautions:
-
presence of allergy
to any of the drugs given
-
fluid and
electrolyte imbalances
-
severe renal
disease
-
caution should be
used with systemic lupus erythematosus (SLE)
-
glucose tolerance
abnormalities or diabetes mellitus
-
gout
-
liver disease
-
pregnancy and
lactation
Adverse effects:
-
the most common
adverse effects seen with diuretics include GI upset, fluid and electrolyte
imbalances, hypotension, and electrolyte disturbances.
Drug- drug interactions:
drugs that altered the actions
of diuretics:
-
antiarrhythmics
(digoxin), drugs that depend on a particular electrolyte balance for their
therapeutic effects.
-
Quinidine, drugs
that depend on urine alkalinity for proper excretion.
-
Antihypertensive
ad antidiabetic agents, depend on normal reflexes to balance their effects.
THIAZIDE AND THIAZIDE- LIKE DIURETICS
-
Hydrochlorothiazide
(hydroDIURIL), the most frequently
used of the thiazide diuretics, often used in combination with other drugs for
the treatment of hypertension.
-
Chlorothiazide
(Diuril), the oldest of this class, and considered the prototype.
-
Bendroflumethiazide
(Naturetin)
-
Hydroflumethiazide
(Diucardin)
-
Methyclothiazide
(Aquatensen)
-
Trichlormethiazide
(Diurese)
*Thiazide- like drugs
-
Chlorthalidone
(Hygroton)
-
Indapamide (Lozol)
-
Metolazole
(Mykrox)
-
Quinethazone
(Hydromox)
Therapeutic actions and indications:
-
Thiazide diuretics
belong to a chemical class of drugs called sulfonamides.
-
Thiazide- like
diuretics has a slightly different chemical structure but work in the same way
that thiazide diuretics do.
-
Their action is to
block the chloride pump.
-
Usually indicated
for the treatment of edema associated with CHF or with liver or renal disease.
-
Also used as
monotherapy or as adjuncts for the treatment of hypertension.
Pharmacokinetics:
-
onset of action:
1-3 hours
-
metabolize in the
liver and excreted in the urine
-
well absorbed in
the GI tract
Contraindications and cautions:
-
contraindicated
with allergy to thiazides or sulfonamides, fluid or electrolyte imbalances and
renal and liver disease.
-
Additional
cautions include: gout, SLE, diabetes, hyperparathyroidism, bipolar disorder,
and pregnancy and lactation.
Adverse effects:
-
Hypokalemia
(weakness, muscle cramps, and arrhythmias)
-
Decrease calcium
excretion, which leads to increase calcium level.
-
Decrease uric acid
excretion (gout, high level of uric acid)
-
Urine will
slightly alkalinized
Drug- drug interactions:
-
decrease
absorption of this drugs if combined with cholestyramine or colestipol, if
combination is used, it should be taken separated by at least 2 hours.
-
Risk of digoxin
toxicity increases due to potential changes in potassium levels; serum
potassium level should be monitored if this combination is used.
-
Decrease
effectiveness of antidiabetic agents may occur related to the changes in
glucose metabolism; dosage adjustment of those agents may be needed.
-
Risk of lithium
toxicity may increase if these drugs are combined. Serum lithium levels should
be monitored and appropriate dosage adjustment made as needed.
LOOP DIURETICS
-work in the loop in henle
-
Furosemide (Lasix),
most common less powerful than new loop diuretics.
-
Bumetanide (Bumex)
-
Torsemide
(Demadex)
-
Ethacrynic acid
(Edecrine)
Therapeutic action and indications:
-
referred to as
high-ceiling diuretics because they cause greater degree of diuresis.
-
Block the chloride
pump in the ascending loop of henle, where normally 30% of all filtered sodium
is reabsorbed.
-
These drugs work
even in the presence of acid- base disturbances, renal failure, electrolyte
imbalances, or nitrogen retention.
-
A drug of choice
when rapid and extensive diuresis is needed.
-
In case of severe
edema, it is important to remember that these drugs can have an effect only on
the blood the nefron.
-
In pulmonary
edema, this fluid then circulates back to the lungs pulls fluid out of the
interstitial spaces by its oncotic pull, and delivers fluid to the kidneys
where the water is pulled out completing the cycle.
-
Commonly indicted
for treatment of acute CHF, pulmonary edema, edema associated with CHF or with
renal or liver disease and hypertension.
Pharmacokinetics:
-
metabolized and
excreted through urine.
-
They should not be
used during pregnancy, unless the benefit to the mother far outweigh the
potential risk, it enters in the breastmilk.
-
Safety for use in
children younger than 18 years of age, has not been establish.
-
If one of this
drug is used for a child, carefully monitor child’s fluid and electrolyte
balance is needed.
Contraindication and cautions:
-
allergy to loop
diuretics, electrolyte depletion, anuria, severe renal failure, hepatic coma,
pregnancy and lactation.
-
Caution on patient
with SLE, gout, and/or diabetes mellitus.
Adverse effect:
-
hyperkalemia is a
very common adverse effect.
-
Alkalosis (a drop
in serum pH to an alkaline state.)
-
Hypotension,
dizziness, ototoxicity, deafness.
-
This may occur in
conduction of fragile nerve in CNS.
Drug- drug interactions:
-
risk for
ototoxicity increase with amino glycosides or cysplapin.
-
Anticoagulation
effect may increase with anticoagulant.
-
Decrease loss of
sodium and decrease antihypertensive effect with indomethacin, ibuprofen,
salicylates, or another NSAIDs.
CARBONIC ANHYDRASE INHIBITOR
-
relatively mild
diuretics.
-
Used to treat
glaucoma
Acetazolamide
(Diamox)
Methazolamide
(Meptazane)
Therapeutic Actions and Indication
-
the enzyme carbonic anhydrase is a catalyst for the formation of sodium
bicarbonate.
-This
diuretics lacks the effects of carbonic anhydrase that slows down the movement
of hydrogen ions, as a result more sodium and bicarbonate are lost in the urine
-
Use as a drug adjuncts to other diuretics when a more intense diuresis is
needed
-
Acetalozamide is used to treat mountain sickness
Pharmacokinetics
-rapidly
absorbed widely distributed excreted in the urine
-
another method of feeding the infant should be used if one of this drugs is
needed during lactation.
Contraindicaions and Cautions
-Allergy to drugs or
antibacterial sulfunamides or thyazide or chronic noncongestive angle closure
glaucoma
-cautios
use is recommended in patients who are breastfeeding, who have fluid imbalances,
renal or hepatic disease, adrenocortical insufficiency, respiratory acidosis or
COPD
Adverse Effects
-
metabolic acidosis
-
hypokalemia
-
paresthesias
(tingling), confusion and drowsiness
Drug to Drug Interaction
- there maybe an increase
excretion of salicylates and lithium if they are combined with this drugs
Potassium- Sparring Diuretics
-
These drugs are
used for patients wha are at risk for hypokalemia associated with diuretic use.
-
Retain potassium
instead of wasting it.
Amiloride
(Midamore)
Spironolactone
(Aldactone)
Triamterene
(Dyrenium)
Therapeutic Actions and Indication
-
These drugs are
often used as adjuncts with thiazide or loop diuretics.
-
Spironolactone is the drug of choice for
treating hyperaldosteronism, a condition seen in cirrhosis of the liver and
nephronic syndrome.
Pharmacokinetics
-
These drugs are
well absorbed, protein bound and widely distributed.
-
These drugs cross
the placenta and enter breast milk.
Contraindicaions and Cautions
-
Allergy to the
drug
-
Hyperkalemia
-
Renal disease
-
Anuria
-
Patients who are
taking Amiloride or triamterene
Adverse Effects
-
Hyperkalemia
OSMOTIC DIURETICS
-
Pull water into
the renal tubule without sodium loss.
-
Drug of choice for
Increase cranial pressure or acute renal failure.
Glycerin (osmoglyn)
Mannidol (Osmitrol)
Urea (ureaphil)
Therapeutic Actions and Indication
-
It acts to pull
large amounts of fluid into the urine by the osmotic pull of the large sugar
molecule.
-
These drugs are
often used in acute situation .
-
Prevent oliguric
phase of renal failure, and to promote of toxic substances through the
kidneys.
Pharmacokinetics
-
These drugs are
freely filtered at the renal glomerulus, poorly reabsorbed by the renal tubules
and not secreted by the tubule, and resistant to metabolism.
Contraindications and Cautions
-
Renal disease and
anuria from sever renal disease, pulmonary congestion, intracranial bleeding,
dehydration and CHF.
Adverse Effects
-
Sudden drop of
fluid levels
-
Cardiac
decompensation and even shock
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Chapter
52- Drugs affecting the Urinary Tract and the Bladder
Urinary Tract
Anti-Infectives
DRUGS:
2 types: antibiotics
& anti infectives works to acidify
the urine
Antibiotics
·
Cinoxacin(Cinobac)-
interferes with the DNA replication in gram negative bacteria
·
Norfloxacin
(Noroxin)- a newer and more broad spectrum drug, is effective against even more
gram negative strains than cinoxacin
·
Fosfomycin
(Monurol)- has the convenience of only one dose. It is not recommended for
patients younger than 18 years of age
·
Nalidixic
(NegGram)- is an older drug that is not effective against as many strains of
gram-negative bacteria as the other antibiotics used for UTIs
·
Nitrofurantion
(Furadantin)- is another older drug with a very short half-life (20-60 minutes)
Anti-infective
works to acidify urine
·
Methenamine
(Hiprex)- undergoes metabolism in the liver and is excreted in the urine
·
Methylene
blue (Urolene Blue)- is widely distributed, metabolized in the tissues, and
excreted in urine, bile, and feces
ACTION:
The urinary anti-infectives act specifically within
the urinary tract to destroy bacteria, either through a direct antibiotic
effect or through acidification of the urine.
PHARMACOKINETICS:
Because these drugs are from several different
chemical classes, the pharmacokinetic data are different for each drug.
CONTRAINDICATIONS:
These drugs are contraindicated in the presence of
any of these drugs. They should be used with caution in the presence of renal
dysfunction, which could interfere with
the excretion and action of these drugs, and with pregnancy and lactation
because of the potential for adverse
effects on the fetus or neonate.
ADVERSE
EFFECTS:
·
nausea,
vomiting, diarrhea, anorexia, bladder irritation, and dysuria
·
infrequent
symptoms include pruritus, urticaria, headache, dizziness, nervousness, and
confusion
·
GI
irritation caused by the agent, which is
alleviated if drug is taken with food
DRUG-DRUG
INTERACTIONS:
Drug
interactions that can occur are very specific to the drug being used.
Urinary Tract
Antispasmodics
DRUGS:
·
Flavoxate
(Urispas)- prevent smooth muscle spasm specifically in the urinary tract, but
it is associated with CNS effects (blurred vision, dizziness, confusion) that
make it less desirable to use in certain patients
·
Oxybutynin
(Ditropan)- is a potent urinary antispasmodic, but it has numerous
anticholinergic effects, making it undesirable in certain conditions or
situations that might be aggravated by decreased sweating, urinary retention,
tachycardia, and changes in the GI activity.
·
Tolterodine
(Detrol,Detrol LA)- is a newer agent that blocks muscarinic receptors,
preventing bladder contraction and spasm
·
Trospium
(Sanctura)- is the newest drug approved to block urinary tract spasms. It also
specifically blocks muscarinic receptors and reduces the muscle tone of the
bladder. It is specifically indicated for the treatment of overactive bladder
with symptoms of urge urinary incontinence, urgency, and urinary frequency.
ACTION:
Inflammation in the urinary tract, such as cystitis,
prostatics, urethritis, and euthrocystitis/urethrotrigonitis, causes smooth
muscle spasms along the urinary tract. Irritation of the urinary tract leading
to muscle spasm also occurs in patient with neurologic bladder.
PHARMACOKINETICS:
These
drugs are rapidly absorbed, widely distributed, metabolized in the liver, and
excreted in urine. Caution should be used in the presence of hepatic or renal
impairment because of the potential of alterations in metabolism or excretion
of the drugs.
CONTRAINDICATIONS:
These
drugs are contraindicated in the presence of any allergy to these drugs; with
pyloric or duodenal obstruction or recent surgery because anticholinergic
effects can cause serious complications.
ADVERSE
EFFECTS:
·
adverse
effects of urinary antispasmodics are related to blocking of the
parasympathetic system
·
nausea
and vommitng, dry mouth, nervousness, tachycardia, and vision changes
DRUG-DRUG
INTERACTIONS:
Decreased
effectiveness of phenothiazines and haloperidol has been associated with the
combination of these drugs with oxybutynin. If any such combinations must be
used, the patient should be monitored closely and appropriate dosage
adjustments made.
Urinary Tract
Analgesic
DRUGS:
·
Phenazopyridine
(Azo-Standard, Baridium, and others) is a dye that is used to relieve pain.
ACTION:
When phenazopyridine is excreted in urine, it exerts
a direct, topical analgesic effect on the urinary tract mucosa. It is used to
relieve symptoms related to urinary tract irritation from infection, trauma, or
surgery.
PHARMACOKINETICS:
Phenazopyridine
is rapidly absorbed and has a very rapid onset of action. It is widely
distributed, crossing the placenta and entering breast milk. It is metabolized
in the liver and excreted in the urine.
CONTRAINDICATIONS:
This
drug is contraindicated in the presence of any allergy to the drug and serious
renal dysfunction, which would interfere with the excretion and effectiveness
of the drug.
ADVERSE
EFFECTS:
·
GI
upset, headache, rash, reddish-orange coloring of urine
·
Hepatic
toxicity, this drug should not be used for longer than 2 days because the toxic
effects may be increased.
DRUG-DRUG
INTERACTIONS:
The risk
of toxic effects of this drug increases if it is combined with anti-bacterial
agents used for treating UTIs. If this combination is used, the phenazopyridine
should not be used for longer than 2 days.
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Chapter 53 – Introduction to the Respiratory System
The
respiratory system’s function is to supply
the blood
with oxygen
in order
for the blood
to deliver
oxygen
to all parts
of the body.
The respiratory system does this
through breathing, thus allowing gas exchange to occur. The normal
functioning of the respiratory system depends on an intricate balance of the
nervous system, cardiovascular, and musculoskeletal systems. It is composed of
two parts namely the upper respiratory tract and the lower respiratory
tract.
THE UPPER RESPIRATORY TRACT
The upper respiratory tract or conducting airways is
composed of the nose, mouth, pharynx, larynx, trachea, and the upper bronchial
tree. In here, air usually moves into the body through nose and into nasal
cavity. The structures of the upper respiratory tract are moist with mucus
(which are produced by the goblet cells in the epithelial lining of the nasal
cavity) and are lined with cilia
(microscopic hair-like projections of the cell membrane). The cilia constantly
move and direct mucus and any trapped substances down toward the throat.
Pairs of sinuses (air-filled spaces, communicating
with the nasal cavity, within the bones of the skull and face) open
into the nasal cavity. From the sinus, the mucus drains into the throat and is
swallowed into the gastrointestinal tract, where stomach acid destroys foreign
materials.
Air moves from the nasal cavity into the pharynx and
larynx. The larynx contains the vocal chords and the epiglottis (which closes
during swallowing). From the larynx, air proceeds to the trachea, the main
conducting airway to the lungs. The trachea divides into two main bronchi,
which further divide into smaller and smaller branches. These bronchial tubes
are composed of three layers: cartilage, muscle, and epithelial cells. All of
these tubes contain mucus-producing goblet cells and cilia. The cilia in these
tubes moves the mucus up to the trachea and into the throat, where again it is
swallowed.
The walls of the trachea and conducting bronchi are
highly sensitive to irritation. When receptors in the walls are stimulated, a
central nervous system reflex is initiated and a cough reflex results, which
causes air to be pushed through the bronchial tree to clean out any foreign
irritant. This reflex, along with the sneeze reflex, forces foreign materials
directly out of the system.
Around the airways, many macrophage scavengers
freely move about the epithelium and destroy invaders. Mast cells are present
in abundance and release histamine, serotonin, and adenosine triphosphate
(ATP), and other chemicals to ensure rapid and intense inflammatory reaction to
any cell injury. The end result of these various defense mechanisms is that the
lower respiratory tract is virtually sterile-an important protection against
respiratory infection that could interfere with essential gas exchange.
THE LOWER RESPIRATORY TRACT
The lower respiratory tract is composed of the
smallest bronchioles and alveoli which both are the functional units of the
lungs. Within the lungs are network of bronchi, alveoli, and blood vessels. The
lung tissue receives its blood supply from the bronchial artery, which branches
directly off the aorta. The alveoli receives unoxygenated blood from the right
ventricle via the pulmonary artery. This delivery of blood to the alveoli is
referred to as perfusion.
Gas exchange or ventilation occurs in the alveoli
where carbon dioxide is lost from the blood and oxygen is to the blood. The
alveolar sac holds the gas, allowing needed oxygen to diffuse across the
respiratory membrane into the capillary while carbon dioxide, which is more
abundant in the capillary blood, diffuses across the membrane and enters the
alveolar sac to be expired.
The respiratory membrane is made up of the capillary
endothelium, the capillary basement membrane, the interstitial space, and the
surfactant layer. The sac is able to stay open because of the surface tension
of the cells is decreased by the lipoprotein surfactant which is produced by
the type II cells in the alveoli. Absence of surfactant leads to alveolar
collapse.
The oxygenated blood is returned to the left atrium
via the pulmonary veins; from there it is pumped throughout the body to deliver
oxygen to the cells and to pick up waste products.
RESPIRATION
The central nervous system controls the respiration
or the act of breathing. The respiratory center in the medulla stimulates the
inspiratory muscle to contract, it also receives input from chemoreceptors and
increase the rate of depth and/or rate of respirations to maintain homeostasis.
The vagus nerve, a predominantly parasympathetic
nerve, plays a key role in stimulating diaphragm constriction and inspiration.
Vagal stimulation also leads to bronchoconstriction or tightening. The
sympathetic system also innervates the respiratory sytem by increasing rate and
depth of respiration and dilation of the bronchi.
RESPIRATORY PATHOLOGY
UPPER RESPIRATORY TRACT CONDITION
·
The Common
Cold
Common
cold is caused by a number of different viruses that invade the upper
respiratory tract, initiating the release of histamine and prostaglandins and
causing an inflammatory response. As a result, mucous membranes become engorged
with blood, the tissues swell, and the goblet cells increase the production of
mucus. These effects cause the person to complain sinus pain, nasal congestion,
runny nose, sneezing, watery eyes, scratchy throat, and headache. In
susceptible, this swelling can block the outlet of Eustachian tube, which may
lead to an ear infection (otitis media).
·
Seasonal
Rhinitis
Seasonal rhinitis or commonly called as hay fever
occurs when the upper airways respond to specific antigen with vigorous
inflammatory response, resulting in nasal congestion, sneezing, stuffiness, and
watery eyes.
·
Sinusitis
Sinusitis occurs when the epithelial lining of the
sinus cavities becomes inflamed. The resultant swelling often causes severe
pain. The danger of sinus infection is that, if left untreated, microorganisms
can move up the sinus passages and into brain tissue.
Pharyngitis
and Laryngitis
Pharyngitis and Laryngitis are infections frequently caused by common bacteria
or viruses. These conditions are frequently seen with influenza.
LOWER RESPIRATORY TRACT CONDITIONS
·
Atelectasis
Atelectasis,
the collapse of once-expanded lung tissue, can occur as a result of outside
pressure against the alveoli or pleural effusion. Atelectasis most commonly
occurs as a result of airway blockage, which prevents air from entering the
alveoli, keeping the lung expanded. This condition occurs when a mucus plug,
edema of the bronchioles, or a collection of pus or secretions occludes the
airway and prevents movement of air. Patients may present rales, dyspnea,
fever, cough, hypoxia, and changes in chest wall movement.
·
Pneumonia
Pneumonia is an inflammation of the lungs caused
either by bacterial or viral invasion of the tissue or by inspiration of
foreign substances into the lower respiratory tract. The respiratory tract
leads to a localized swelling, engorgement, and exudation of protective sera.
The respiratory membrane is affected, resulting in decreased gas exchange.
Patients complain of difficulty breathing and fatigue, and they present with
fever and noisy breath sounds, and poor oxygenation.
·
Bronchitis
Acute bronchitis occurs when bacteria, viruses, or
foreign materials infect inner layer of the bronchi. The person with bronchitis
may have a narrowed airway during the inflammation; this condition can be very
serious in a person with obstructed or narrowed airflow. Chronic the bronchi
that does not clear.
·
Bronchiectasis
Bronchiectasis is a chronic disease that involves
the bronchi and bronchioles. It is characterized by dilation of the bronchial
tree and inflammation of the bronchial passages. With chronic inflammation, the
bronchial epithelial cell membranes, combined with the dilation of the
bronchial tree, leads to chronic infections in the now unprotected lower areas
of the lung tissue. Patients with this condition often have an underlying
medical condition that makes them more susceptible to infections. Patients
present with the signs and symptoms of acute infection, including fever,
malaise, myalgia, arthalgia, and a purulent, productive cough.
Obstructive Pulmonary Diseases
·
Asthma
It is characterized by reversible bronchospasm,
inflammation and hyperactive airways. The hyperactivity is triggered by
allergens or nonallergic inhaled irritants or by factors such as exercise and
emotions. The triggers cause an immediate release of histamine, which result in
bronchospasm in about 10 minutes. The later response (3 to 5 hours) is
cystokine-mediated inflammation, mucus production, and edema contributing to
obstruction. The extreme case of asthma is the status asthmaticus which can be
life-threatening because bronchospasm does not respond to usual treatment and
occludes air flow into the lungs.
·
Chronic
Obstruction Pulmonary Disease (COPD)
COPD is a permanent, chronic obstruction of airways,
often related to cigarette smoking. It is caused by two related disorders,
emohysema and chronic bronchitis. Emphysema is characterized by loss of elastic
tissue of the lungs, destruction of the alveolar walls, and a resultant hyperinflation
and tendency to collapse with expiration. Chronic bronchitis is a permanent
inflammation of the airways with mucus secretion, edema, and poor inflammatory
defenses. Persons with COPD are characterized by both disorders.
·
Cystic
Fibrosis
Cystic fibrosis is a hereditary disease that results
in the accumulation of copious amounts of very thick secretions in the lungs.
Eventually, the secretions obstruct the airways, leading to destruction of the
lung tissue. Treatment is aimed at keeping the secretions fluid and moving and
maintaining airway patency as much as possible.
·
Respiratory
Distress Syndrome (RDS)
Respiratory distress syndrome is frequently seen in
premature babies whose lungs are not yet fully developed and their surfactant
levels are still very low. Surfactant is necessary for lowering the surface
tension in the alveoli so that they can stay open to allow the flow of gases.
Treatment is aimed at instilling surfactant to prevent atelectasis and to allow
the lungs to expand. Adult respiratory distress syndrome (ARDS) is
characterized by progressive loss of lung compliance and increasing hypoxia.
This syndrome occurs as a result of severe insult to the body.
lui
Chapter 54- Drugs Acting on the Upper Respiratory Tract
These drugs work to keep the airways open and gas to move freely.
Ø Antitussives- blocks
the cough reflex
Ø Decongestants- decrease
the blood flow to the upper respiratory tract and decrease the overproduction
of secretions
Ø Antihistamines- block
the release or action of histamine, a chemical released during inflammation
that increases secretions and narrows airways.
Ø Expectorants- increase
productive cough to clear the airways.
Ø Mucolytics- increase or
liquefy respiratory secretions to aid the clearing of the airways.
Antitussives
-
Drugs that suppress the cough reflex.
-
Act directly on the medullary cough center of the brain to depress the cough
reflex.
-
Acts as a local anesthetic on the respiratory passages, lungs, and pleurae,
blocking the effectiveness of the stretch receptors that stimulate a cough
reflex.
-
Contraindicated for patients w/ postoperative and those who have undergone
abdominal or thoracic surgery.
-
Caution should be used in patients who are hypertensive or have a history of
addiction to narcotics
- T ½ of 2-4
hrs; metabolized in liver and excreted in urine
-
Side effects include: dizziness, respiratory depression and dry mouth
Drugs in this class:
benzonatate(Tessalon);
codeine(generic); P dextromethorpan(Benylin); hydrocodone(Hydocan)
Implemetation:
-
teach the pt. the proper administration of the drug to ensure therapeutic
effect
-
caution pts. not to use the drug longer than 5 days to facilitate detection
of the underlying medical conditions that may require treatment.
-
provide safety measures if dizziness occurs to prevent patient injury
-
offer support and encouragement to help the patient cope with the disease
and the drug regimen
Decongestants
-
Drugs that cause local vasoconstriction
-
Decrease the blood flow to the irritated and dilated capillaries of the mucous
membranes lining the nasal passages and sinus cavities.
- Topical Nasal Congestants
-
are sympathomimetics
-
cause vasoconstriction, leading to decreased edema and inflammation of the
nasal membranes
-
caution in patients with lesions or erosions in the mucous membranes.
-
T ½ of 0.4-0.7 hr; absorbed systematically, metabolized in the liver and
excreted in the urine.
-
Side effects include: disorientation, confusion, light headedness, nausea,
vomiting, fever, dyspnea, rebound congestion
Drugs in this class: P ephedrine(Kondon’s
Nasal); oxymetazoline(Afrin, Allerest); phenylephrine(Coricidin);
trahydrozoline(Tyzine); xylometazoline(Otrivin)
- Oral Decongestants
-decrease nasal congestion
related to common colds,sinusitis,and allergic rhinitis.
-relieve pain and congestion
of otitis media
- shrink the nasal
mucous membrane by stimulating the alpha-adrenergic receptors in the nasal
mucus membrane,promoting drainage of the sinuses and improving air flow.
-Pseudoephedrine peak levels-
20 to 45 minutes.
-ask the patient to void
before taking the drug.
-contraindicated to patient
with glaucoma,hypertension,diabetes,thyroid disease,coronary disease and
prostate problems.
-Adverse effects: rebound
congestion,anxiety,tenseness tremors,hypertension,arrythmias,sweating,and
pallor.
-encourage patient not to use
this drug for more than 1 week.
- Topical Nasal Steroid Decongestants
-
treatment for allergic rhinitis,been found to be effective in patient that
doesn’t respond with other decongestants.
-
Has an anti-inflammatory action that produce direct local effect.
-
Onset of action may not be immediate, and may require up to a week to cause any
changes.
-
If no effects after 3 weeks , discontinue the drug.
-
Relieve inflammation after removal of nasal polyps.
-
Contraindicated with Candida Albicans infection,caution to those with TB,chickenpox,and
measles.
Drugs in this class: P
flunisolide, Beclomethasone (Beclovent), Budesonide (Rhinocort) ,Dexamethasone
(Decaderm),Fluticasone (AeroBid),Triamcinolone ( Kenacort)
Antihistamines
-blocks the effect of
histamine 1 receptor sites, bringing relief to the patient to patients
suffering from itchy eyes,swelling,congestion,and drippy nose.
-treatment for seasonal and
perennial allergic rhinitis,uncomplicated urticaria,angioedema
-also has anticholinergic
effects and antipruritic effect.
-most effective if used
before the onset of symptoms.
-Onset of action 1-3 hours.
-caution to those with
arrythmias and prolonged Q-T intervals.
-Adverse effects: drying of
the respiratory and GI mucous membranes,GI upset , nausea,dysuria,urinary
hesitancy,and skin eruption and itching associated with dryness.
-increase effect if taken
with MAOI, ketoconazole,and erythromycin.
-administer drug in an empty
stomach
-have patient void before
each dose
-Avoid alcohol
Drugs in this class: P
Diphenhydramine (Benadryl) T ½ of 2.5-7 hours
1st generation:
Azelastine (Astelin),Brompheniramine, Buclizine ( Bucladin
S),Cetirizine(Reactine),Chlorpheniramine (Aller-chlor),Clemastine
(Tavist),Cyclizine (Marezine),Cyproheptadine(Periactin),Dexclorpheniramine(Dexchlor),Dimenhydrinate
(Dimentabs),Hydroxyzine
(Vistaril),Meclizine (Bonine),Phenindamine (Nolohist),Promethazine(Phenergan).
2nd generation :
Desloratadine (Clarinex),Fexofenadine (Allegra),Loratadine ( Claritin).
Expectorants
-liquefy lower respiratory
tract secretions,reducing viscosity of these secretions, and making it easier
for patient to cough them out.
-reduces adhesiveness and
surface tension of secretions,movement of less viscous secretions
-more productive cough,
decreased frequency of coughing.
-P Guaifenesin
(symptomatic reliefof respiratory condition characterized by dry,
nonproductive, cough, and in the presence of mucus in respiratory cough)
-adverse effects:
Nausea,vomiting,headache,dizziness,rash.
-Not
to use this drug for more than 1 week.
-Advise the use of
small,frequent meals.
Mucolytics
-aid in high –risk respiratory patient in coughing up thick
secretions,tenacious secretions.
-for COPD, cystic
fibrosis,pneumonia,tuberculosis,atelectasis,diagnostic
bronchoscopy,
Postoperative patients with tracheostomy.
-administer through instillations or nebulization.
-caution with acute brochospasm,peptic ulcer,and esophageal varices.
-splits links in mucoproteins contained in secretions,decreasing viscosity.
Drugs in this class : P Acetylcysteine (Mucomyst) T ½ 6.25 hr ,Dornase alfa
(Pulmozyme)
Chapter 55 - Drugs Used To Treat Obstructive Pulmonary
Disease
Bronchodilators/
Antiasthmatics-dilating airways
Xanthines
-main treatment for
bronchospasm and asthma.
-has direct effect
on the smooth muscles of respiratory tract,both in the bronchi and in the blood
vessels.
- stimulate 2
prostaglandins resulting in smoothe muscle relaxation, which then increase the vital capacity.
- inhibit the SRSA.
- Unlabeled use:
stimulation in respiration Cheyne Stokes respiration.
- Peak levels within
2 hours.
- Caution with
patient with GI problems,coronary disease,respiratory dysfunction,renal or
hepatic lung disease,alcoholism,hyperthyroidism.
- Increases with nicotine.
Drugs in the class: P
Theophylline ( Sio-bid ,Theo Dur)
T ½ of 3-15 hr (nonsmoker),4-5 hr
(smoker),
Aminophylline(Truphylline), Caffeine, Dyphylline (Dilor).
-administer drug with food or
milk.
Sympathomimetics
-mimic the effects of the
sympathetic nervous system.
-dilates the bronchi and
increased the rate and depth of respiration.
-beta2 selective
adrenergic agonists.
-Adverse effects: increase
BP,HR,vasoconstriction,decreased renal and GI bloodflow.
-rapidly absorb after injection.
Half life of < 1 hour.
-Caution on those with cardiac
disease,vascular disease,diabetes,hyperthyroidism, pregnancy and lactation
- avoid combination with bronchodilators,general anesthetics
cyclopropane,and halogenated hydrocarbon.
- administer with small frequent
meals.
Drugs in this class: P Epinephrine (Sus –Phrine, EpiPen), Albuterol(Proventil),
Bitolterol (Tornalate), Ephedrine,Formoterol (Foradil), Isoetharine(Bronkosol),
Isoproterenol (Isuprel), Levalbuterol (Xopenex), Metaproterenol (Alupent).
Anticholinergic
Bronchodilators
-not as effective as
sympathomimetics but can provide some relief to those patient who could not
respond to other drugs.
-has an effect in the vagus
nerve,which block or antagonize the action of the neurotransmitter
acetylcholine at vagal-mediated receptor sites, leading to relaxation of smooth
muscles by bronchodilation.
Drugs in this class: P
Ipratropium with an onset of action of 15 minutes when inhaled.Peak of
1-2 hours,Thiotropium has rapid onset and longer duration with half life
of 5 to 6 days.
-Encourage client to void before
each dose.
-Provide small frequent meals and
sugarless lozenges.
-Caution patient not to use
inhalator for more than 12 inhalations in 24 hours.
Inhaled Steroids
-very effective for treatment of
bronchospasm.
-decrease inflammatory response
in the airway,thus increasing air flow and facilitate respiration.
-Has 2 effects:
Ø
Decreased swelling associated with inflammation and promotion in the beta
–adrenergic receptor activity.
Ø
Inhibit bronchoconstriction.
-used for prevention and
treatment of asthma,treat chronic steroid-dependent bronchial asthma.
-should be taken 2-3 weeks to
achieve effects.
-Adverse effects: sore
throat,coughing,dry mouth,and pharyngeal and laryngeal fungal infection.
-have patient use decongestant
drops before using inhaled steroid.
-Have patient rinse his mouth
after inhaler.
Drugs in this class include:P
Flunisolide (AeroBid) T ½ of 1-2 hours., beclomethasone (beclovent),Budesonide
(Pulmicort),Fluticasone (Flovent),Triamcinolone (Azmacort).
Leukotriene Receptor
Anatagonist
-selectively,and competitively
blocks the receptor for production of leukotrienes D4 ,E4 components
of SRSA.
-blocks many signs and symptoms
of asthma,such as neutrophil,eosinophil migration,neutrophil,and monocyte
aggregation,leukocyte adhesion,increased capillary permeability,and
smooth muscle contraction.
-prophylaxis for bronchial asthma
and in patients younger than 12 years of age.Not indicated for treatment of
acute asthma attack.
-metabolized via cytochrome P450
and excreted in feces.
-Abverse effects:
headache,dizziness,myalgia,nausea,diarrhea,elevated liver
enzymes,vomiting,fever,pain.
-Increased toxicity if taken with
propanolol,theophylline,and warfarin
Drugs in this class : P
Zafirlukast (Accolate),Montelukast(Singulair),Zileuton (Zyflo).
-administer drug in an empty
stomach.
-Caution patient not to stop meds
in symptom –free periods.
Lung Surfactant
-naturally occurring substance
lipoproteins containing lipids, and apoproteins that reduce the surface tension
within the alveoli for gas exchange.
-used to replace the surfactant
that is missing in lungs of neonates with RDS.
-begin to act immediately on
instillation into the trachea.
-No contraindications
-Adverse effects: patent ductus
arteriosus in infants,hypotension,intraventricular
hemorrhage,pneumothorax,pulmonary air leak,hyperbilirubinemia,and sepsis.
Drugs in this class: P Beractant
(Survanta),Calfactant(Infasurf),Colfosceril (Exosurf, Neonatal ),
Poractant (Curosurf).
-suction the infant immediately
before administration,but do not suction for 2 hours after administration.
Mast Cell Stabilizers
-prevent release of inflammatory
and bronchoconstricting substances when mast cells are stimulated to release
these substances because irritation.
Drugs in this class: P Cromolyn T
½ of 80 min(inhibit release of histamine and SRSA,and is inhaled in a
capsule but may not reach its peak effect for 1 week).Nedocromil (inhibit
mediators of inflammatory cells including
eosinophils,neutrophils,macrphages,and mast cells.
-treatment of mild-moderate
bronchial asthma of >12 years old patients.
-Cromolyn not recommended for
children younger than 2 years old,and nedocromil not recommended for children
younger than 12.
-Adverse effects:
headache,dizziness,nausea,sore throat,dysuria,cough and nasal congestion.
-Administer oral drug 30 minutes
before meals and at bedtime.
-Instruct patient not to
wear contact lenses if using Cromolyn eye drops.
-Dizziness and fatigue common
problem in takinh Nedocromil.
CHAPTER 56 – INTRODUCTION TO THE GASTROINTESTINAL SYSTEM
The gastrointestinal (GI) system
is the only system in the body that is open to the external environment. The GI
system is composed of one continuous tube that begins at the mouth; progresses
through the esophagus, stomach and small and large intestines; and ends at the
anus. The pancreas, liver and gallbladder are accessory organs that support the
functions of the GI system.
Composition of the
Gastrointestinal Tract
The GI tube is composed of four layers:
- The Mucosa – provides the inner lining of the GI
tract
- The Muscularis Mucosa – is made up of muscles. It
helps the tube open and squeezing the tube to aid digestion and motility.
It also helps propel the gastrointestinal contents down the tract.
- The Nerve Plexus – these gives the GI tract local
control of movement, secretions, and digestion.
- The Adventitia – outer layer of the GI tract, serves
as a supportive layer and helps the tube maintain its shape and stay in
position.
Gastrointestinal Activities
The system has four major
activities:
- Secretion
- Absorption
- Digestion
- Motility
Secretion – secretes various
compounds to aid the movement of the food bolus through the GI tube, to protect
the inner layer of the GI tract from injury and to facilitate the digestion and
absorption of nutrients.
-
Saliva – contains water and digestive enzymes
and facilitate swallowing by making bolus slippery
-
Histamine 2 receptors – gastrin and
parasympathetic system stimulates it, causing the cells to release hydrochloric
acid into the lumen of the stomach.
-
Bile – contains detergent like substance that
breaks apart fat molecules so that they can be processed and absorbed.
-
Gallstones – develop when the concentrated bile
crystallizes.
Digestion – process of breaking
food into usable, absorbable nutrients.
Absorption – active process of
removing water, nutrients and other elements from the GI tract and delivering
them to the bloodstream for use for the body.
Motility – GI tract depends on
this to keep things moving through the system.
-
Peristalsis – basic movement in the esophagus.
It is a constant wave of contraction that moves from the top to the bottom of
the esophagus.
-
Swallowing – response to a food bolus in the
back of the throat stimulates the peristaltic movement that directs the food
bolus into the stomach.
-
Segmentation – involves contraction of one
segment of small intestine while the next segment then relaxes, and the relaxed
segment contracts.
Local Gastrointestinal Reflexes
·
Gastroenteric reflex: stimulatiuon of the
stomach by stretching, the presence of food, or cephalic stimulation causes an
increase in activity in the small intestine. It is thought that this prepares
the small intestine for the coming chyme.
·
Gastrocolic reflex: stimulation of the stomach
also causes increased activity in the colon, again preparing to empty any
contents to provide space for the new chime.
·
Duodenal-colic reflex: the presence of food or
stretch in the duodenum stimulates colon activity and mass movement, again to
empty the colon for the new chime.
Other local GI reflexes:
·
Ileogastric reflex
·
Intestinal-intestinal reflex
·
Peritoneointestinal reflex
·
Renointestinal reflex
·
Vesicointestinal reflex
·
Somatointestinal reflex
Central Reflexes
Two
centrally mediated reflexes - Swallowing reflex and Vomiting reflex – are very
important to the functioning of the GI tract.
Ø
Swallowing – is a centrally mediated reflex that
is important in delivering food to the GI tract for processing. It is
controlled by the medulla and involves a complex series of timed reflexes.
Ø
Vomiting – is controlled by the chemoreceptor
trigger zone (CTZ) in the medulla or by the emetic zone in immature or injured
brains. The CTZ is stimulated by several different processes and initiates a
complex series of responses that first prepare the system for vomiting and then
cause a strong backward peristalsis to rid the stomach of its contents.
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