Post on 07-Jul-2018
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ackground
Nearly all forms of acute glomerulonephritis have a tendency to progress to chronic
glomerulonephritis. The condition is characterized by irreversible and progressive
glomerular and tubulointerstitial fibrosis, ultimately leading to a reduction in the
glomerular filtration rate (GFR) and retention of uremic toins. !f disease progression isnot halted "ith therapy, the net results are chronic #idney disease ($%&), end'stage renal
disease (R&), and cardiovascular disease. $hronic glomerulonephritis is the third
leading cause and accounts for about *+ of all causes of $%&.
The eact cause of $%& in patients "ith chronic glomerulonephritis may never be #no"nin some patients. Therefore, it has generally been accepted that the diagnosis of $%& can
be made "ithout #no"ledge of the specific cause.-*
The National %idney Foundation (N%F) defines $%& on the basis of either of the
follo"ing/
vidence of #idney damage based on abnormal urinalysis results (eg, proteinuria or
hematuria) or structural abnormalities observed on ultrasound images 0 GFR of less than 1+ m23min for 4 or more months
!n accordance "ith this definition, the N%F developed guidelines that classify the progression of renal disease into five stages, from #idney disease "ith a preserved GFR
to end'stage #idney failure. This classification includes treatment strategies for each
progressive level, as follo"s/
tage * – This stage is characterized by #idney damage "ith a normal GFR (≥ 5+
m23min)6 the action plan consists of diagnosis and treatment, treatment of comorbidconditions, slo"ing of the progressing of #idney disease, and reduction of
cardiovascular disease ris#s
tage 7 – This stage is characterized by #idney damage "ith a mild decrease in the
GFR (1+'5+ m23min)6 the action plan is estimation of the progression of #idney
disease
tage 4 – This stage is characterized by a moderately decreased GFR (to 4+'85
m23min)6 the action plan consists of evaluation and treatment of complications
tage 9 – This stage is characterized by a severe decrease in the GFR (to *8'75
m23min)6 the action plan is preparation for renal replacement therapy tage 8 – This stage is characterized by #idney failure6 the action plan is #idney
replacement if the patient is uremic
0t the later stages of glomerular in:ury, the #idney are small and contracted and biopsy
results cannot help distinguish the primary disease. ;istology and clues to the etiology
are often derived from other systemic diseases (if present). $onsiderable cause'specific
variability is observed in the rate at "hich acute glomerulonephritis progresses to chronicglomerulonephritis.
http://emedicine.medscape.com/article/777272-overviewhttp://emedicine.medscape.com/article/777272-overviewhttp://emedicine.medscape.com/article/984358-overviewhttp://emedicine.medscape.com/article/1918879-overviewhttp://emedicine.medscape.com/article/1918879-overviewhttp://emedicine.medscape.com/article/javascript:showrefcontent('refrenceslayer');http://emedicine.medscape.com/article/777272-overviewhttp://emedicine.medscape.com/article/984358-overviewhttp://emedicine.medscape.com/article/1918879-overviewhttp://emedicine.medscape.com/article/1918879-overviewhttp://emedicine.medscape.com/article/javascript:showrefcontent('refrenceslayer');
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The prognosis depends on the type of chronic glomerulonephritis (see tiology). R&
and death are common outcomes unless renal replacement therapy is instituted.
Pathophysiology
Reduction in nephron mass from the initial in:ury reduces the GFR. This reduction leads
to hypertrophy and hyperfiltration of the remaining nephrons and to the initiation of intraglomerular hypertension. These changes occur in order to increase the GFR of theremaining nephrons, thus minimizing the functional conse
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Dembranoproliferative glomerulonephritis/ ' 0bout 9+ of patients "ith
membranoproliferative glomerulonephritis progress to $RF and R& in *+ years !g0 nephropathy – 0bout *+ of patients "ith !g0 nephropathy progress to $RF
and R& in *+ years -4
@oststreptococcal glomerulonephritis ' 0bout *'7 of patients "ith poststreptococcal
glomerulonephritis progress to $RF and R&6 older children "ho present "ithcrescentic glomerulonephritis are at greatest ris#
2upus nephritis – Everall, about 7+ of patients "ith lupus nephritis progress to
$RF and R& in *+ years6 ho"ever, patients "ith certain histologic variants (eg,class !C) may have a more rapid decline
Epidemiology
!n the >nited tates, chronic glomerulonephritis is the third leading cause of R& andaccounts for *+ of patients on dialysis.
!n apan and some 0sian countries, chronic glomerulonephritis has accounted for asmany as 9+ of patients on dialysis6 ho"ever, subse
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@ericardial friction rub in pericarditis
Tenderness in the epigastric region or blood in the stool (possible indicators of
uremic gastritis or enteropathy)
&ecreased sensation and asteriis (indicators of advanced uremia)
Complications
The presence of the follo"ing complications generally indicates a need for urgent
dialysis/
Detabolic acidosis
@ulmonary edema
@ericarditis
>remic encephalopathy
>remic gastrointestinal bleeding
>remic neuropathy
evere anemia and hypocalcemia
;yper#alemia
DD
The presence of the follo"ing complications generally indicates a need for urgentdialysis/
Detabolic acidosis
@ulmonary edema
@ericarditis
>remic encephalopathy
>remic gastrointestinal bleeding
>remic neuropathy
evere anemia and hypocalcemia
;yper#alemia
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Laboratory Studies
Urinalysis
The presence of dysmorphic red blood cells (R=$s), albumin, or R=$ casts suggests
glomerulonephritis as the cause of renal failure. Aay or broad casts are observed in all
forms of chronic #idney disease ($%&), including chronic glomerulonephritis. 2o"urine'specific gravity indicates loss of tubular concentrating ability, an early finding in
persons "ith $%&. ee >rinalysis.
Urinary protein excretion
>rinary protein ecretion can be estimated by calculating the protein'to'creatinine ratioon a spot morning urine sample. The ratio of urinary protein concentration (in mg3d2) to
urinary creatinine (in mg3d2) reflects 79'hour protein ecretion in grams. For instance, if
the spot urine protein value is 4++ mg3d2 and the creatinine value is *8+ mg3d2, the
protein'to'creatinine ratio is 7. Thus, in this eample, the 79'hour urine protein ecretionis 7 g.-?
The estimated creatinine clearance rate is used to assess and monitor the glomerular
filtration rate (GFR). The 7 formulas available for calculation of the GFR are the
$oc#croft'Gault formula, "hich estimates creatinine clearance, and the Dodification of &iet in Renal &isease (D&R&) tudy formula, "hich is used to calculate the GFR
directly.
The $oc#croft'Gault formula is simple to use but overestimates the GFR by *+'*8
because creatinine is both filtered and secreted. The D&R& formula is much morecomple but can be determined "ith a smartphone and tablet application available from
the National %idney Foundation or can be calculated online through the ;ypertension,&ialysis, and $linical Nephrology Aeb site.
The estimated creatinine clearance rate is also used to monitor response to therapy and toinitiate an early transition to renal replacement therapy (eg, dialysis access placement and
transplantation evaluation). The degree of proteinuria, especially albuminuria, helps
predict the renal prognosis in patients "ith chronic glomerulonephritis. @atients "ith
proteinuria eceeding * g3day have an increased ris# of progression to end'stage renalfailure.
Complete blood count
0nemia is a significant finding in patients "ith some decline in the GFR. @hysicians must be a"are that anemia can occur even in patients "ith serum creatinine levels lo"er than 7
mg3d2. ven severe anemia can occur at lo" serum creatinine levels. 0nemia is the result
of mar#ed impairment of erythropoietin production.
Serum chemistry
erum creatinine and urea nitrogen levels are elevated. !mpaired ecretion of potassium,
free "ater, and acid results in hyper#alemia, hyponatremia, and lo" serum bicarbonate
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levels, respectively. !mpaired vitamin &'4 production results in hypocalcemia,
hyperphosphatemia, and high levels of parathyroid hormone. 2o" serum albumin levels
may be present if uremia interferes "ith nutrition or if the patient is nephrotic. Recently, ahigh fibroblast gro"th factor 7* (FGF7*) "as found to be significantly elevated in
patients "ith $%& and the high levels of FGF7* may eplain the ecess overall and
cardiovascular mortality in patients "ith $%&. These adverse effects of elevated FGF7*are not clearly understood but research is under"ay to elucidate its biologic effects.
ther Studies!enal ultrasonography
Ebtain a renal ultrasonogram to determine renal size, to assess for the presence of both
#idneys, and to eclude structural lesions that may be responsible for azotemia. mall#idneys often indicate an irreversible process.
"idney biopsy
!f the #idney is small, #idney biopsy is usually unnecessary6 no specific pattern of disease
can be discerned at this point. 0 #idney biopsy may be considered in the minority of patients "ho ehibit an acute eacerbation of their chronic disease. This may be
particularly pertinent to patients "ith preserved #idney size and in those "ith lupus
nephritis.
!n early stages, the glomeruli may still sho" some histologic evidence of the primarydisease. !n advanced stages, the glomeruli are hyalinized and obsolescent. The tubules are
disrupted and atrophic, and mar#ed interstitial fibrosis and arterial and arteriolar sclerosis
occur.
#pproach Considerations@atients "ith chronic #idney disease ($%&) "ho are admitted to the hospital should
receive careful monitoring of "eight, inta#e, output, and renal function so that acute renalfailure (0RF) can be diagnosed and treated early if it occurs,. 0ll potentially nephrotoic
agents must be ad:usted for the degree of $%&. Furthermore, agents such as nonsteroidal
anti'inflammatory drugs (N0!&s), aminoglycosides, and intravenous (!C) contrast
media must be avoided unless the benefits clearly out"eigh the ris#s6 they are stronglyassociated "ith 0RF.
@rogression from $%& to end'stage renal disease (R&) can be slo"ed by a variety of
measures, including aggressive control of diabetes, hypertension, and proteinuria. &ietary
protein restriction, phosphate restriction, and hyperlipidemia control may have significantimpact on retarding disease progression.
pecific therapies for some glomerular diseases (eg, lupus) should be implemented in
appropriate settings. 0ggressively manage anemia and renal osteodystrophy (eg,
hyperphosphatemia, hypocalcemia, or hyperparathyroidism) before initiating renalreplacement therapy. 0lso, aggressively manage comorbid conditions, such as heart
disease and diabetes.
http://emedicine.medscape.com/article/2054430-overviewhttp://emedicine.medscape.com/article/2054430-overview
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Nephrotic patients (urinary protein ecretion 4.8 g3day) may have hyperlipidemia. 0s a
part of cardiovascular health care, the lipid profile should be chec#ed, and lipid'lo"ering
therapy should be started for patients "ith hyperlipidemia.
teroid therapy may induce or eacerbate diabetes, hypertension, "eight gain, fatredistribution in the trun# (buffalo hump) and face (moon facies), cosmetic problems (eg,
hirsutism and acne), and osteoporosis.
Donitor fasting blood glucose levels and blood pressure. Ebtain baseline bone
densitometry values. Repeat bone densitometry for bone pain. Eral calcium supplements(* g3day) and vitamin & (9++'B++ !>3day) are recommended for prophylais against
osteoporosis.
Pharmacologic $herapy lood pressure management
The target blood pressure for patients "ith proteinuria in ecess of * g3day is less than*783?8 mm ;g6 for patients "ith proteinuria of less than * g3day, the target pressure is
less than *4+3B+ mm ;g.
0ngiotensin'converting enzyme inhibitors (0$!s) are commonly used and are usually
the first choice for treatment of hypertension in patients "ith chronic #idney disease($%&). 0$!s are renoprotective agents that have additional benefits beyond lo"ering
pressure. They effectively reduce proteinuria, in part by reducing the efferent arteriolar
vascular tone, thereby decreasing intraglomerular hypertension.
!n particular, 0$!s have been sho"n to be superior to conventional therapy in slo"ing
the decline of the glomerular filtration rate (GFR) in patients "ith diabetic and
nondiabetic proteinuric nephropathies. Therefore, 0$!s should be considered for treatment of even normotensive patients "ith significant proteinuria.-B
The role of angiotensin !! receptor bloc#ers (0R=s) in renal protection is increasingly
being established, and these medications have been found to retard the progression of $%& in patients "ith diabetic or nondiabetic nephropathy, much as 0$!s do.-5
0 combination of 0$! therapy and 0R= therapy has been sho"n to achieve better
pressure control and preservation of renal function than either therapy alone could.
Therefore, in patients "ithout hyper#alemia or an acute rise in serum creatinine levelsafter the use of either therapy, combination therapy should be attempted.-*+
;o"ever, in patients "ith vascular disease or diabetes, combination 0$! and 0R=therapy has been associated "ith increased adverse effects, including hyper#alemia,
"orsening renal function, and mortality. 0s such, combination 0$! and 0R= therapy
should not be used to treat hypertension in these groups of patients "ith $%&.-**
&iuretics are often re
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and 0R=s. ;o"ever, they should be used "ith caution "hen given together "ith 0$!s
or 0R=s because the decline in intraglomerular pressure induced by 0$!s or 0R=s may
be eacerbated by the volume depletion induced by diuretics, potentially precipitating0RF.
=eta bloc#ers, calcium channel bloc#ers,-*7 central alpha7 agonists (eg, clonidine),
alpha* antagonists, and direct vasodilators (eg, minoidil and nitrates) may be used to
achieve the target pressure.
%ibrosis inhibition
=ecause progressive fibrosis is the hallmar# of chronic glomerulonephritis, some
investigators have focused on finding inhibitors of fibrosis in an attempt to slo"
progression. Ef the many compounds that have been considered, pirfenidone, an inhibitor of transforming gro"th factor beta and hence of collagen synthesis, has emerged as the
best candidate.
$ho et al, in an open'label study involving 7* patients "ith idiopathic and postadaptive
focal segmental glomerulosclerosis, found that pirfenidone yielded a median 78improvement in the rate of decline of the estimated GFR6 the drug did not affect
proteinuria or blood pressure.-*4 0mong the adverse events attributed to therapy "ere
dyspepsia, sedation, and photosensitive dermatitis. !t is hoped that pirfenidone therapy
"ill prove an effective means of slo"ing progressive fibrosis6 ho"ever, more studies areneeded.
!ole o& antioxidants 'bardoxolone(
$ells have the ability to produce antioidants, anti'inflammatory and detoifyingenzymes that are useful for cell viability, but this path"ay is constantly being inhibited by
an enzyme called %0@. !nhibition of %0@ may therefore improve the antioidant
activity of cells and promote cell viability. =ardoolone, an oleanolic acid derivative, bloc#s %eap and has been postulated as a potential mechanism to retard progression of $%&. !n one study, patients receiving bardoolone had significant increases in the mean
(H standard deviation) estimated GFR, as compared "ith placebo, at 79 "ee#s. The
improvement persisted at 87 "ee#s, suggesting that bardoolone may have promise for the treatment of $%&, ho"ever a phase 4 randomized clinical trial failed to achieve the
primary end point and "as associated "ith side effects and so the study "as stopped. -*9 !t
is not li#ely that =ardoolone "ill be used for renoprotection any time soon.
!ole o& sodium bicarbonate
odium bicarbonate has been sho"n to reduce tubulointerstitial in:ury and endothelin
production "ith substantial benefits in slo"ing progressive #idney damage. !n one studyon patients "ith advanced #idney failure, the administration of sodium bicarbonate preserved GFR decline.-*9 ven in patients "ith relatively preserved GFR in stage 7
$%&, the administration of sodium bicarbonate "as sho"n to preserve #idney function
over 8 years.-*8 0 study in patients "ith stage 9 $%& found that * year of consuming adiet that included fruits and vegetables dosed to reduce dietary acid by half had effects
comparable to those of daily oral sodium bicarbonate at *.+ m
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!ole o& direct renin inhibitors
@reliminary studies using alis#iren,-*? a direct renin inhibitor, sho" reductions in proteinuria over 1 months, but larger studies did not sho" benefit.
)anagement o& other problems
Renal osteodystrophy can be managed early by replacing vitamin & and by administering
phosphate binders. ee# and treat nonuremic causes of anemia, such as iron deficiency, before instituting therapy "ith erythropoietin.
Treat hyperlipidemia (if present) to reduce overall cardiovascular comorbidity, even
though evidence for lipid lo"ering in renal protection is lac#ing.
!enal !eplacement $herapy&iscuss options for renal replacement therapy (eg, hemodialysis, peritoneal dialysis, and
renal transplantation).
0rrange permanent vascular access "hen the GFR falls belo" 7+'78 m23min, "hen theserum creatinine level eceeds 9 mg3d2, or "hen the rate of increase in the serum
creatinine level indicates the need for dialysis "ithin * year. 0rteriovenous fistulas are preferred to arteriovenous grafts because of their long'term high'patency rates and should
be placed "henever possible. @lace peritoneal dialysis catheters 7'4 "ee#s before
anticipated dialysis therapy.
@reemptive transplantation before the initiation of dialysis results in better survival thantransplantation after the initiation of dialysis. Therefore, preemptive transplantation
should be eplored from live donors. @atients "ithout live donors can be placed on the
deceased donor "ait list "hen the GFR falls belo" 7+ m23min to accrue time. @atients"ho opt for no treatment "hen it is indicated should be informed of imminent renal
failure in a shorter time.
pose patients to educational programs for early rehabilitation from dialysis or
transplantation.
Consultations
@atients "ith any evidence of #idney disease should be referred to a #idney specialist (ie,
a nephrologist). arly referral of patients "ith $RF (serum creatinine, *.8'7 mg3d2) to a
nephrologist is important for managing complications and organizing the transition torenal replacement therapy. ome evidence indicates that early referral of $RF patients to
a nephrologist improves the short'term outcome. The nephrologist "ill usually determine
the fre
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@rotein'restricted diets (+.9'+.1 g3#g3day) are controversial but may be beneficial in
slo"ing the decline in the GFR and reducing hyperphosphatemia (serum phosphate 8.8
mg3d2) in patients "ith serum creatinine levels higher than 9 mg3d2. Donitor these patients for signs of malnutrition, "hich may contraindicate protein restriction. ducate
patients about ho" potassium'rich diets help control hyper#alemia. Dany dietary
restrictions are no longer necessary "ith the initiation of renal replacement therapy.
ncourage patients to increase their activity level as tolerated. !ncreased activity may aidin blood pressure control.
!n obese patients "ith mild to moderate $%&, "eight loss may help reverse renal
dysfunction, manifesting as reduction in proteinuria and albuminuria.-*B, *5
)edication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Dedications used to treat chronic glomerulonephritis include angiotensin'converting
enzyme (0$) inhibitors (0$!s), diuretics, calcium channel bloc#ers, beta'adrenergic
bloc#ers, and alpha'adrenergic agonists.
#CE ,nhibitors
Class Summary
0$!s are renoprotective agents. They decrease intraglomerular pressure and,
conse
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decreases intraglomerular pressure and glomerular protein filtration by decreasing
efferent arteriolar constriction.Cie" full drug information
ena0epril 'Lotensin(
=enazepril prevents conversion of angiotensin ! to angiotensin !!, a potent
vasoconstrictor, resulting in increased levels of plasma renin and a reduction inaldosterone secretion.
!t decreases intraglomerular pressure and glomerular protein filtration by decreasing
efferent arteriolar constriction.Cie" full drug information
%osinopril
Fosinopril is a competitive 0$ inhibitor. !t prevents conversion of angiotensin ! to
angiotensin !!, a potent vasoconstrictor, resulting in increased levels of plasma renin and
a reduction in aldosterone secretion. !t decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.Cie" full drug information
1uinapril '#ccupril(
Iuinapril is a competitive 0$ inhibitor. !t reduces angiotensin !! levels, decreasingaldosterone secretion. !t decreases intraglomerular pressure and glomerular protein
filtration by decreasing efferent arteriolar constriction.
*iuretics. Loop
Class Summary
&iuretics are used to treat edema and hypertension. They increase urine ecretion by
inhibiting sodium and chloride transporters.Cie" full drug information
%urosemide 'Lasix(
Furosemide is the diuretic of choice. !t increases ecretion of "ater by interfering "ith
the chloride'binding cotransport system, "hich, in turn, inhibits sodium and chloride
reabsorption in the ascending loop of ;enle and the distal renal tubule. Cie" full druginformation
umetanide ' umex(
=umetanide increases the ecretion of "ater by interfering "ith the chloride'binding
cotransport system, "hich, in turn, inhibits sodium, potassium, and chloride reabsorptionin the ascending loop of ;enle. These effects increase the urinary ecretion of sodium,
chloride, and "ater, resulting in profound diuresis. Renal vasodilation occurs after administration, renal vascular resistance decreases, and renal blood flo" is enhanced. !nterms of effect, * mg of bumetanide is e
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ascending loop of ;enle and distal renal tubule. This agent is used only in refractory
cases. $ontinuous !C infusion is preferable in many cases. !t is indicated for temporary
treatment of edema associated "ith heart failure "hen greater diuretic potential is needed.
*iuretics. $hia0ide
Class Summary
&iuretics are used to treat edema and hypertension. They increase urine ecretion by
inhibiting sodium and chloride transporters.
Cie" full drug information
)etola0one '/aroxolyn(
Detolazone treats edema in congestive heart failure. !t increases ecretion of sodium,
"ater, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal
tubules. !t may be more effective in cases of impaired renal function.Cie" full druginformation
Hydrochlorothia0ide ')icro0ide(
;ydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased
ecretion of sodium and "ater as "ell as potassium and hydrogen ions.
Calcium Channel lockers
Class Summary
$alcium channel bloc#ers are used to treat hypertension, angina, and atrialfibrillation.Cie" full drug information
#mlodipine '2or+asc(
0mlodipine bloc#s slo" calcium channels, causing relaation of vascular smooth
muscles.Cie" full drug information
2i&edipine 'Procardia(
Nifedipine relaes coronary smooth muscle and produces coronary vasodilation, "hich,
in turn, improves myocardial oygen delivery. ublingual administration is generallysafe, theoretical concerns not"ithstanding.Cie" full drug information
%elodipine
Felodipine relaes coronary smooth muscle and produces coronary vasodilation, "hich,
in turn, improves myocardial oygen delivery. !t benefits nonpregnant patients "ithsystolic dysfunction, hypertension, or arrhythmias. !t can be used during pregnancy if
clinically indicated.
$alcium'channel bloc#ers potentiate 0$ inhibitor effects. Renal protection is not
proven, but these agents reduce morbidity and mortality rates in congestive heart failure.
$alcium channel bloc#ers are indicated in patients "ith diastolic dysfunction. They areeffective as monotherapy in blac# patients and elderly patients.Cie" full drug information
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,sradipine '*ynaCirc(
!sradipine is a dihydropyridine calcium channel bloc#er. !t inhibits calcium from enteringselect voltage'sensitive areas of vascular smooth muscle and myocardium during
depolarization. This causes relaation of coronary vascular smooth muscle, "hich results
in coronary vasodilation. Casodilation reduces systemic resistance and blood pressure,
"ith a small increase in resting heart rate. !sradipine also has negative inotropiceffects.Cie" full drug information
Verapamil (Calan, Isoptin, Verelan)
&uring depolarization, verapamil inhibits calcium ions from entering slo" channels and
voltage'sensitive areas of vascular smooth muscle and myocardium. !t can diminish
premature ventricular contractions (@C$s) associated "ith perfusion therapy anddecrease ris# of ventricular fibrillation and ventricular tachycardia. =y interrupting re'
entry at the 0C node, it can restore normal sinus rhythm (NR) in patients "ith
paroysmal supraventricular tachycardias.Cie" full drug information
*iltia0em 'Cardi0em. *ilacor 3!. *ilt0ac. )at0im L#(
&uring depolarization, diltiazem inhibits calcium ions from entering slo" channels and
voltage'sensitive areas of vascular smooth muscle and myocardium.
eta4 lockers. eta45 Selecti+e
Class Summary
=eta'adrenergic bloc#ers compete "ith beta'adrenergic agonists for available beta'
receptor sites. These agents inhibit mainly beta* receptors (located mainly in cardiacmuscle).Cie" full drug information
)etoprolol 'Lopressor. $oprol 3L(
Detoprolol is a selective beta*'adrenergic bloc#er that decreases the automaticity of contractions. &uring intravenous (!C) administration, carefully monitor blood pressure,
heart rate, and electrocardiographic readings.Cie" full drug information
isoprolol '/ebeta(
=isoprolol is a selective beta*'adrenergic receptor bloc#er that decreases automaticity of contractions.Cie" full drug information
Esmolol ' re+ibloc(
smolol is an ultra–short'acting beta7'bloc#er. !t is particularly useful in patients "ithlabile arterial pressure, especially if surgery is planned, because it can be discontinuedabruptly if necessary. !t may be useful as a means to test beta'bloc#er safety and tolerance
in patients "ith a history of obstructive pulmonary disease "ho are at possible ris# of
bronchospasm from beta'bloc#ade. The elimination half'life of esmolol is 5minutes.Cie" full drug information
#tenolol '$enormin(
http://reference.medscape.com/drug/isradipine-342376http://reference.medscape.com/drug/calan-sr-isoptin-sr-verapamil-342380http://reference.medscape.com/drug/calan-sr-isoptin-sr-verapamil-342380http://reference.medscape.com/drug/cardizem-cd-diltiazem-342374http://reference.medscape.com/drug/cardizem-cd-diltiazem-342374http://reference.medscape.com/drug/lopressor-toprol-xl-metoprolol-342360http://reference.medscape.com/drug/lopressor-toprol-xl-metoprolol-342360http://reference.medscape.com/drug/monocor-zebeta-bisoprolol-342367http://reference.medscape.com/drug/monocor-zebeta-bisoprolol-342367http://reference.medscape.com/drug/brevibloc-esmolol-342358http://reference.medscape.com/drug/brevibloc-esmolol-342358http://reference.medscape.com/drug/tenormin-atenolol-342356http://reference.medscape.com/drug/tenormin-atenolol-342356http://reference.medscape.com/drug/isradipine-342376http://reference.medscape.com/drug/calan-sr-isoptin-sr-verapamil-342380http://reference.medscape.com/drug/calan-sr-isoptin-sr-verapamil-342380http://reference.medscape.com/drug/cardizem-cd-diltiazem-342374http://reference.medscape.com/drug/cardizem-cd-diltiazem-342374http://reference.medscape.com/drug/lopressor-toprol-xl-metoprolol-342360http://reference.medscape.com/drug/lopressor-toprol-xl-metoprolol-342360http://reference.medscape.com/drug/monocor-zebeta-bisoprolol-342367http://reference.medscape.com/drug/monocor-zebeta-bisoprolol-342367http://reference.medscape.com/drug/brevibloc-esmolol-342358http://reference.medscape.com/drug/brevibloc-esmolol-342358http://reference.medscape.com/drug/tenormin-atenolol-342356http://reference.medscape.com/drug/tenormin-atenolol-342356
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0tenolol selectively bloc#s beta'* receptors "ith little or no effect on beta'7 receptors.
Beta4Blockers. 2onselecti+eClass Summary
Nonselective beta'bloc#ers inhibit both beta* receptors (located mainly in cardiac
muscle) and beta7 receptors located in the bronchial and vascular musculature. Theseagents slo" the sinus rate and decrease 0C nodal conduction. $arefully monitor blood
pressure.
Cie" full drug information
Propranolol ',nderal L#. ,nnoPran 3L(
@ropranolol is a class !! antiarrhythmic nonselective beta'adrenergic receptor bloc#er. !t
has membrane'stabilizing activity and decreases the automaticity of contractions.Cie"
full drug information
Sotalol ' etapace. Sorine(
This class !!! antiarrhythmic agent bloc#s %J channels, prolongs action potential duration
(0@&), and lengthens the IT interval. !t is a non–cardiac selective beta'adrenergic bloc#er. otalol is sho"n to be effective in the maintenance of sinus rhythm, even in patients "ith underlying structural heart disease.Cie" full drug information
Labetalol '$randate(
2abetalol bloc#s alpha', beta*', and beta7'adrenergic receptor sites, decreasing blood
pressure.Cie" full drug information
Penbutolol
@indolol has mild intrinsic sympathomimetic activity and negative chronotropic andinotropic effects.Cie" full drug information
Penbutolol 'Le+atol(
@enbutolol has mild intrinsic sympathomimetic activity and negative chronotropic andinotropic effects.
#lpha4 lockers. #ntihypertensi+es
Class Summary
0lpha* antagonists may be used to achieve the target pressure. @eripheral alpha'
antagonists inhibit postsynaptic alpha'adrenergic receptors, resulting in vasodilation of veins and arterioles and decreasing total peripheral resistance and blood pressure. These
drugs often cause mar#ed hypotension after the first dose. ;igh doses are li#ely to cause
postural hypotension. Ef the peripheral alpha'antagonists, doazosin and terazosin are
selective for alpha* 6'receptors. @razosin is nonselective and inhibits both alpha*' andalpha7'receptors.Cie" full drug information
*oxa0osin 'Cardura. Cardura 3L(
http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/trandate-labetalol-342359http://reference.medscape.com/drug/trandate-labetalol-342359http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/cardura-xl-doxazosin-342343http://reference.medscape.com/drug/cardura-xl-doxazosin-342343http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/betapace-af-sotalol-342365http://reference.medscape.com/drug/trandate-labetalol-342359http://reference.medscape.com/drug/trandate-labetalol-342359http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/levatol-penbutolol-342370http://reference.medscape.com/drug/cardura-xl-doxazosin-342343http://reference.medscape.com/drug/cardura-xl-doxazosin-342343
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&oazosin, a
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#lpha7 #gonists. Central4#cting
Class Summary
0lpha'adrenergic agonists are used in combination "ith other agents for management of
hypertension.Cie" full drug information
Clonidine 'Catapres. *uraclon. 2exiclon 3!(
$lonidine stimulates presynaptic (central) alpha7'adrenergic receptors, thereby reducing
norepinephrine release and peripheral vasoconstriction.
http://reference.medscape.com/drug/catapres-tts-clonidine-342382http://reference.medscape.com/drug/catapres-tts-clonidine-342382http://reference.medscape.com/drug/catapres-tts-clonidine-342382http://reference.medscape.com/drug/catapres-tts-clonidine-342382