Danil
hammoudi.md
Sinoe
medical association
Cardio-pharmacology:
ANTIANGINAL
DRUGS
***NITRATES AND NITRITES:
1. -NITROGLYCERINE
2. -AMYL
NITRITE
3. -PENTAERTHRITOL
TETRANITRATE
4. -ISOSORBITE
DINITRATE
*** BETA ADRENERGIC BLOCKING DRUGS:
-CARDIOSELECTIVE
: +++ACEBUTOLOL
+++ATENOLOL
+++METOPROLOL
***CALCIUM CHANEL BLOCKERS
-NIFEDIPINE
-VERAPAMIL
-DILTIAZEM
ANTIHYPERTENSIVE DRUGS:
1/THIAZIDES: ***CHLOROTHIAZIDE
***HYDROCHLOROTHIAZIDE
2/SYMPATHOLYTIC
AGENTS:
+++CLONIDINE
+++GUANABENZ
+++GUANFACINE
***PERIPHERAL
ACTING:
·
BETA ADRENERGIC BLOCKING AGENTS : PROPANOLOL.
·
ALPHA ADRENERGIC BLOCKING AGENT :+++PRAZOSIN
+++TERASOZIN
+++RESERPINE
+++GUANETHIDINE
+++GUANADREL
·
ARTERIAL VASODILATATORS:
+++HYDRALAZINE
3/ANGIOTENSINE CONVERTING ENZ:
+++(ACE)
INHIBITORS
+++CAPTOPRIL
+++ENALPRIL
+++LISINOPRIL
4/CALCIUM CHANNEL BLOKERS:
+++NIFEDIPINE
+++VERAPAMIL
+++DILTIAZEM
5/DRUG FOR HYPERTENSIVE EMERGENCIES:
+++TRIMETHAPEN
+++SODIUM
NITROPRUSSIDE
+++DIAZOXIDE
+++NIFEDIPINE
+++LABETALOL
PRAZOSIN:
·
QUINAZOLINE DERIVATIVE
·
SELECTIVE BLOCKER OF POSTSYNAPTIC ALPHA1 RECEPTORS BLOCKING
AGENT THAT CAUSES VASODILATATION OF BOTH ARTERIES AND VEINS.
·
REDUCES VASCULAR TONE IN BOTH RESISTANCE AND CAPACITANCE
VESSELS
·
CAUSES A SMALL DEGREE OF TACHYCARDIA
·
CAUSES VASODILATATION IN BOTH ARTERIES AND VEINS
·
HIGHLY BOUND TO PLASMA PROTEIN
·
IT DOES NOT INCREASE PLASMA RENIN ACTIVITY
·
FLUID RETENTION OCCUR DURING LONG TERM THERAPY
·
REDUCE PERIPHERAL VASCULAR RESISTANCE AND LOWERS ARTERIAL
BLOOD PRESSURE IN BOTH SUPINE AND ERECT PATIENT
INDICATION: MODERATE HTA
ACUTE
CONGESTIVE HEART FAILURE
ADVERSE
EFFECT: DIZINESS ,HEADACHE,
DROWSINESS, PALPITATION
POSTURAL
HYPOTENSION AND SYNCOPE
TESTS
FOR ANTINUCLEAR FACTOR MAY BECOME POSITIVE.
CAPTOPRIL
ENALAPRIL
LISINOPRIL
-Antagonist of the renin angiotensine system by inhibition
of PEPTIDYL DIPEPTIDASE [ANGIOTENSINE CONVERTING ENZ (ACE)].
-The CAPTOPRIL block the enzymatic conversion of
angiotensine I to angiotensine II=ACE INHIBITORS.
1***THESE AGENT
ARE NOT ANGIOTENSINE II ANTAGONISTS, NOR DO THEY POSSESS AGONIST ACTIVITY.
2***THEY REDUCE
SYSTEMIC BLOOD PRESSURE IN PATIENTS WITH INCREASED ANGIOTENSINE I LEVELS BUT
NOT IN NORMAL INDIVIDUALS WHO ARE IN NA+ BALANCE.
3***When
administration orally, these agents reduce blood pressure in hypertensive
patient with high, normal or low plasma RENIN levels
4***Many
hypertensive patients with normal Renin level respond to CAPTOPRIL, which
suggests that other factors affecting the RENIN ANGIOTENSINE SYSTEM [NA+,
DEPLESION] may have a role in hypertension.
-These agents also increase the actions of BRADYKININ, since
it is inactivated by PEPTIDYL DIPEPTIDASE.
-THEY ARE ABLE TO DEPRESS THE SECRETION OF ALDOSTERONE BY
LOWERING ANGIOTENSINE II PRODUCTION.
CHEMISTRY: IS HYDROLYZED IN THE LIVER
MECHANISM OF ACTION:
INHIBIT VASOCONSTRICTION [ANGIOTENSINE
II--->VASOCONSTRICTION]
ANGIOTENSINE II STIMULATES THE SECRETION OF ALDOSTERONE,
WHICH PROMOTES SALT AND WATER RETENTION
CAPTOPRIL INHIBIT SALT, WATER RETENTION AND SLIGHTLY
INCREASE SERUM K+ LEVELS.
THE PEPTIDYL DEPEPTIDASE IS NECESSARY TO CATALYZE THE
DEGRADATION OF BRADYKININ.
THE ACE INHIBITORS MAY INCREASE THE CONCENTRATION OF
BRADYKININ, WHICH IS A PROTEIN VASODILATATOR.
THE ACE INHIBITORS ALSO EXERT AN ANTIHYPERTENSIVE EFFECT IN
LOW RENIN HYPERTENSION,
THE MECHANISM OF ACTION IN THIS CASE IS NOT EXPLAINED
.
PHARMACOCINETICS:
CAPTOPRIL: ***RAPIDLY ABSORBED FOLLOWING ORAL ADMINISTRATION
***REACHES
PEAK BLOOD LEVEL WITHIN AN HOUR
***95% OF A
DOSE IS ELIMINATED BY THE KIDNEYS WITHIN 24H
ENAPRIL: ***ITS DURATION OF ACTION IS MORE THAN 24H DUE TO ITS HEPATIC
CONVERSION AND ACTIVATION .
***ENAPRIL
DOES NOT REACH CLINICALLY ACTIVE LEVELS FOR 2-4 HOURS, BUT IT HAS A 1/2 LIFE 11 HOURS.
LISINOPRIL: ***IS ABSORBED MORE SLOWLY THAN ENAPRIL
***HAS A
SLOWER ONSET OF ACTION
PHARMACOLOGIC
EFFECTS:
CARDIOVASCULAR EFFECTS : ***REDUCTION IN TOTAL
PERIPHERAL RESISTANCE [ARTERIAL BLOOD PRESSURE]
NO
CHANGE IN CARDIAC OUTPUT
THERAPEUTIC USES: ***OFTEN
ADMINISTER WITH THIAZIDE DIURETIC
***AN
ACE INHIBITOR CAN ALSO BE GIVEN WITH A BETA BLOCKER
***HTA
***INSUFFISANCE
CARDIAC CONGESTIVE
ADVERSE
EFFECTS: ***PROTEINURIA
***ACE
INHIBITORS ARE CONTREINDICATED IN PATIENTS
WITH BILATERAL RENAL ARTERY STENOSIS
***HYPOTENSION
***NEUTROPENIA
[PATIENT WITH SERIOUS AUTOIMMUNE DISEASE]
***HEADEACHE,
DIZINESS, AND FATIGUE ARE THE MOST COMMON SIDE EFFECT ASSOCIATED WITH
ENALAPRIL.
***COUGH
AND BRONCHOSPASM
***HYPERKALIEMIA
MECHANISM
OF ACTION OF ANGIOTENSIN
ANGIOTENSIN II ACTS THROUGH SPECIFIC CELLS SURFACE RECEPTORS
LOCATED ON TARGET TISSUES.
RENIN : A JUXTAGLOMERULAR ENZ CONTROLES THE FORMATION OF
ANGIOTENSIN II
ANGIOTENSIN
II: ***VASOCONSTRICTORS
***PRODUCES
POSITIVE INOTROPIC AND CHRONOTROPIC EFFECTS WHICH ARE DUE TO CENTRAL AND
PERIPHERAL SYMPATHETIC STIMULATION.
***STIMULATES
SYMPATHETIC GG AND ENHANCES GANGLIONIC TRANSMISSION
==>
THIS MAY BE MEDIATED BY INCREASED BIOSYNTHESIS OF NOREPINEPHRINE
·
DECREASE REUPTAKE OF NOREPINEPHRINE
·
INCREASE THE RELEASE OF THE NEUROTRANSMITTER
***STIMULATES
THE SYNTHESIS AND SECRETION OF ALDOSTERONE BUT THIS HAVE VERY LITTLE EFFECT ON
BLOOD PRESSURE.
***CAN
STIMULATE THE SECRETION OF ADH, WHEN INJECTED INTRAVENTRICULARLY.
ACETALOZAMIDE
: INHIBIT CARBONIC ANHYDRASE
PRODUCE
A MODEST DIURESIS
HIGH
PH, INCREASED NaHCO3, DECREASED NH4+
LOOP
DIURETIC: FUROSEMIDE
INHIBIT THE
NA+ K+ 2CL- CO TRANSPORT SYSTEM IN THE THICK ASCENDING LIMB OF THE LOOP OF
HENLE==> COPIOUS DIURESIS AND DECREASE FREE WATER CLEARENCE AS WELL AS THE
MEDULLARY OSMOTIC GRADIENT
THIAZIDE:
DIURETIC
ACT AS INHIBITORS OF CA2+ AND NA+ TRANSPORT
ACTING
PRIMARILY IN THE DISTAL NEPHRON
THEY
MAY INCREASE K+ EXCRETION
AMILORIDE: INHIBIT THE EXCHANGE OF NA+ FOR H+ IN
THE PROXIMAL TUBULE TO A SMALL EXTEND AND DECREASE K+ EXCRETION BY BLOCKING NA+
CHANNELS AND THEREBY THE TRANSEPITHELIAL POTENTIAL IN THE DISTAL TUBULE.
ALDOSTERONE
ANTAGONISTS: DECREASE K+ EXCRETION ==> SLIGHT LOSS OF NA+
PHENYLNEPHRINE HAS A HIGHER AFFINITY FOR ADRENORECEPTORS a1.
a1 ADRENERGIC NEUROMEDIATOR OUT PUT IS CONTROLED BY
PRIMARILY OR PRESYNAPTIC NERVE ENDING
DANTROLENE
:
·
TRT MALIGNANT HYPERTHERMIA + CONTROL MANIFESTATION OF SPASTICITY
RESULTING FROM UPPER NEURON DISORDER
·
BLOCK THE RELEASE OF CA++ FROM SARCOPLASMIC RETICULUM OF
MUSCLE CELLS
·
ACT IN THE MUSCLE BY DECREASING CA++ RELEASE FROM THE
SARCOPLASMIC RETICULUM
·
ANTISPASTICITY DRUG
ADVERSE
EFFECT : GENERALIZED SKELETTAL MUSCLE WEAKNESS
BRETYLIUM:
ANTIARRHYTHMIC DRUGS K+ CHANNEL BLOCKER
PIRENZEPINE
: -TREAT PEPTIC ULCER DISEASE IS NOT AN H2 HISTAMINE RECEPTOR
BLOCKER
-ANTIMUSCARINIC AGENT
ATROPINE
AND SCOPOLAMINE : BLOCK OF MUSCARINIC OF THE
PARASYMPATHIC .
LEUCINE =THE
ONLY AMINO ACIDS KETOGENIC
DONOR IN NEUTROGENIC ATOM IN THE UREA FORMATION [UREA CYCLE]
IS : CARBAMOYL PHOSPHATE
AMPHETAMINES IS NOT INCLUDED IN DEPRESSIVE DISEASE, USED IN
:
***NARCOLEPSY
***ANOREXIGENIC
***ATTENTION
DEFICIT
***HYPERKINETIC
DISORDER IN CHILDREN
MORPHINE : CAUSE HYPERPOLARIZATION OF NERVE CELL, INHIBITING
OF NERVE FIRING AND PRESYNAPTIC INHIBITION OF NEUROTRANSMITTER RELEASE.
ANTIOXIDANT:ASCORBATE
VIT E
BETA
CAROTENE
GLUTATHIONE
METOPROLOL
ACTION : BETA BLOCKER
BLOCKER OF BINDING OF A NEUROTRANSMITTER AT
THE BETA 1 ADRENERGIC RECEPTOR WICH DECREASE IN INTRACELLULAR cAMP
AMINOGLYCOSIDE :
OTOTOXICITY AND NEPHROTOXICITY.
LOVASTATIN :
DECREASE BLOOD CHOLESTEROL
INHIBIT
SYNTHESIS OF CHOLESTEROL BY BLOCKING HMG COA REDUCTASE