Zatchot 1 Semester Flashcards
explain the general pharmacology and its parts
-its consist of 2 parts :
1-pharmacodynamic : the effect of the drug on the body ( it has two parts :effect and mechanism)
2-pharmacokinetics : the effect of the body on the drug
it has 4 parts which is :
1-absorption
2-distribution
3-metabolism
4-elimination
explain the Phamacodynamic
-Dif : its the effect of the drug on the body
—once the drug entering the body the drug goes to body control system which is the targets :
1-drug receptor 2- ion channels 3-enzymes ( extra or intra cellular ) 4-transport system ( carrier molecules )
————————————-
-the receptor and its types :
-receptor: its protein micro-molecule embedded in the cell membrane has extra cellular level and intra cellular level
-if the drug bind to receptor called ligands , if the ligand activate the receptor will be called agonist , and if blocked or inhibit the receptor called antagonist
—-types of receptor:
1-ligand gated-ion channel :after binding of agonist or antagonist to ion channels receptor the transmembrane conductance of specific ion increased or decreased and that causing a change in vital activity of cell membrane
2-G protein couples receptor :they are located in cell membrane and they implement there responses through the second massinger and when agonist bind to it a further signal performed and change a number of enzymes in cell or coupled ion channel
3- enzyme linked receptor: usually has extra cellular domain for ligand which is cytokines
and intracellular domain which is
tyrosin kinase
4-receptor regulating gene transcription
receptor regulating gene transcription are termed nuclear receptor
some of them located in the cytoplasm and migrate to nucleus only after binding to ligand
-types of bonds between the drug and receptor:
1-hydrogen bond : like OH bond NH and its reversible
2-ionic bond : opposite charge attract each other , and its reversible
3-covalent bond : its sharing of atoms and becomes 1 unite and its irreversible
–how drugs can effect on :
1-ion channel
2-enzymes
3-carrie molecules ( transporter )
1- ion channels:
1-1 the drug block it physically
1-2 receptor ion channel
1-3 through g-proteins receptor activate it which lead to Camp open the ion channel
——-
2-enzymes:
2-1 the drug goes and bond with enzyme with reversible bond
2-2 irreversible bond like ( Organophosphate)
2-3 false substances: like Ldopa converted to be dopamine, so when the drug interact with the enzyme the enzyme false between the real L dopa and fake L dopa which is the the drug and prevent synthesis of dopamine
———
3- Carrie molecules or transporter :
3-1 increase the carrier molecules or decrease it
explain the - Agonist and antagonist agents
1-Agonist:
-agonist: its substance with affinity and intrinsic activity
- DF of affinity : is the ability of substance to bind to a biological target resulting of formation of substance- receptor complex
- the agonist can reach maximum effect which can be expected from the medicinal agent and that’s called = efficacy
-another term is the potency: which is determined by the concentration in which the substance produced 50% of the effect
— types of the agonist :
1-full agonist : its the ligand that bind to receptor and produce the maximum cellular response
2-partial agonist : its the ligand which bind to the receptor with internisc activity greater then 0 but less the 100%
— type of response in the agonist
1-graded response : its response proportionally related to the dose which mean increasing of the dose will lead to increase of response
2-quintal response :the response about all or non Ex the epilpicy and arethmeia 
- antagonist:
-we have 2 types :
1- comparative antagonist : have affinity but no intrinsic activity ( blocker ) and bind at the same site of agonist
2- non-competitive antagonist : occurs when antagonist occupies which so called allosteric binding site in receptor
(micro molecule non receptor sites which regulate the receptor activity
- other types of antagonist :
1-chemical antagonist: ex mixing acidic drug with alkaline drug
2-physical antagonist: ex patient have a toxicity of (heparin ) which has negative charge so we give him ( protamine ) which has positive charge so they make complex and the body execrating them both
3-pharmacokinetics antagonist ; ex if a patient has anemia and he take medicine for the anemia and then he took a medicine for stomach acid which is ( antacid ) the antacid prevent the absorption of iron which he needed for the anemia so this is a antagonism on level of the absorption
explain the pharmacokinitics all
pharmacokinetics : the effect of the body on the drug
it has 4 parts which is :
1-absorption
2-distribution
3-metabolism
4-elimination
————————
————–1-Absorption
DF : its the passage of the drug from site of administration to the plasma
— main site of administration:
1-oral. 2-sublingual 3-rectal 4-inhalation 5- injection
—- transmembrane movement of the drug :
1-simple diffusion: the most important method of drug absorption
2-filtration: important for drug excretion by kidney
simple and filtration also known as passive transfer
3-active transport
4-facilitated diffusion:
active and facilitated also known as carrier -mediated
5-pinocytosis: its active process which energy dependent in which the drug is engulfed inside the cell pinocytosis and facilitated and active known as specialized transporter
- factors effect the drug absorption:
- there is 2 types of factors
1- factors related to the drug :
1-1 molecular size
1-2 dose : increase of the dose lead to increase of the absorption
1-3 lipid salability ( pKa) : drug ionization
2- factors related to the body :
2-1 route of administration
2-2 integrity of the absorption surface
2-3 blood flow
-The Henderson-Hasselbach Equation ( pKa):
-The Henderson-Hasselbach Equation expresses a relationship between the body compartment pH, the drug’s pKa (can be measured in the laboratory), and provides the ratio of acidic and basic forms of the drug
- clinical significant for pKa:
1- know the site of drug absorption from GIT
2-treatment of toxicity, with acidification or alkalization
Absorption% = Pka-PH
-the ion trap - the ion trap is mean that the drug will ionized in the cell and cant diffuse to the blood stream
-Ex: ion trap for aspirin
the ph pKa for aspirin is 3,5
ph of stomach is 1,5
ph of stomach cell same as plasma which is 7,4 - ## so if patient took a large dose of aspirin with empty stomach the aspirin will move to stomach and bcs both acidic the aspirin will diffuse to stomach cells but becs the stomach cells doesn’t change the ph bcs there is no food the wall stomach get injured could explode , and the patient start vomiting blood , but after a time the ionized aspirin will change chemically and get diffused to blood circulation
——————2-distribution Vd
1— volume of distribution (vd)
Df: the apparent volume if water into which the drug is distributed in the body after distribution equilibrium
- site of drug distribution:
1- plasma 3 L water
2- extracellular 9L water
3-intercellular 29 L water
total 41-42 L water in the whole body
-formula: vd=total amount of drug divided by plasma concentration
—- clinical significant :
-we can know if the patient can be treated with dialysis or not
1- so if its vd less then 5 L it can be dialysis
2- if between 10-15 L its restricted to medical stuff to decide
3 if its more then 41 L then the drug is more bounded to proteins tissue and cannot be removed by dialysis
2-distribution proteins bound:
- Df of binding of the drug to plasma proteins: most drug inter the body are bound to plasma proteins, albumin the most important plasma proteins becs can bind with positive and negative charge drug
- clinical significant : the pharmacological effect of the drug is related only to free part of the drug not the part which bound to plasma proteins
, the part that bound to plasma proteins work as reservoir from which the drug slowly realized
——————-
———————3-metabolism
—Df of metabolism and its main function: transfer the substance that entered the body which is lipid-soluble to water-soluble to be easy excreted
—- the major site of metabolism is the : liver but not the only
——- ceases of drug in the metabolism is 1 of these 4 :
1- active to inactive
2- active to active ex: codein to morphen
3-inactive to active : ex enaloprel to enalaprolant
4- from any shape to toxic: ex paracetamol to in Acitlypenzokinon
We have 2 Phases :
-Phase 1 : - it has 3 types :
1-oxidation ( the important one )
2-reduction
3-hydrolysis
—-Phase 1 oxidation :
happend in the vesicles inside the hepatocytes there is a lot of enzymes group but we are interested in 1 group of them which call ( cytochrome P450 )
its family of enzyme consist of not less then 50 enzyme which is mixed function oxignesis
—- the most valuable enzyme of this family called (CYP3A4) this enzyme can metabolize 50% of the our drugs
—types of microsomal :
1- microsomal inducers : induce the cyp3a4
1-1 barbiturates
1-2 Rifampin
1-3 carbamezoampin
1-4 cigarettes smoking
2- microsomal inhibitors: inhibit CYP3A4
2-1cimatadene
2-2 ketokonzol
2-3 Erythromycin
2-4 grape fruit
——- Ex the contraceptive bills with cigarettes smoking or rifampin ( tuberculosis drug )
-Phase 2 :
-Phase 2 ( conjugated ) : phase 2 activated if chemistry of the drug doesn’t work with phase 1
— mechanism:
if the liver fail to metabolize with first phase , the liver will conjugate the drug with large molecules like acylation , sulfation but most of the time glucuronic acid , in neonates the primary pathway is sulfation , after conjugated with large molecule which is water-soluble the liver will excrete the conjugated molecule through bile then to intestine
—- enzyme inducer or inhibitor : its only available with ( groconail transfers )
- first pass metabolism:
Df : the first place at which drug could be metabolize partly before reaching the systemic circulation
—- cases of First pass metabolism:
1-passing through the liver without in first pass metabolism
2- first pass metabolism of drug partly in the live
3- the liver first metabolize the drug
100 % ex lidocaine ( we should look for another rout of administration)
- Bioavailability:
- its the fraction of the drug that reach the systemic circulation after passing the ( absorption and first pass metabolism )
- formula:
bioavailability=absorption – FPM result by percentage
—————-
——————4-Elimination/ Execration
- elimination = excretion + metabolism
Clearance (Cl, ml/min.) – volume of blood plasma which totally cleared of drug per unit of time
Cl total = Clrenal + Clhepatic + Clother
– Most drugs are eliminated by first-order process. The amount of drug eliminated per unit of time does not remain constant. But fraction of drug eliminated per unit of time remains constant
Half-life – time necessary for the concentration of drug in the plasma to decrease by half
NB! drug eliminated after 4-5 half life
what is the division or classification of Autonomic nervous system drugs
— they are 2
-1-parasympathetic ( cholinergic receptors)
- and this receptors divided into 2
1-muscranic receptor (M) : which follows the mechanism of G-protein receptor
2-Nicotinic Receptors (N) : which follows the Ion channel receptor
-2- Sympathetic ( Adrenergic receptor )
explain the Muscrinc and nectoinc Receptors location and effects
- first of all we need to know that ( Gq ) means: second massinger and thats will :
1- increasing the Calsm
2- decreasing the CMP
and we will refer to it by (+)
—— types of receptor and its location and its effects:
1-M1+ : CNS , (Gastric mucosa , HCL secretion, gall bladder )
2-M2: (heart , bradycardia) + (smooth muscles )
3-M3+:
3-1: bronchial smooth muscles ( bronchi construction)
3-2 : blood vessels ( vasodilation)
3-3: Eye ( Meiosis and gland secretion )
3-4: GIT and urinary ( contractions of the wall and relax of the sphincter)
— there is 2 type of them
1- Nectoinc Neural (Nn) : which found in
1-1 CNS
1-2: Adrenal medulla
1-3: autonomic Ganglion
—and its effect on the heart is :
1- Chronotropy : heart rate
2- Iontropy : force of the contraction
3-Dromotropy: conduction of electrical impulse through ( Av node )
————
2-Nectonic Muscular ( Nm) which found in the skeletal muscles
classification of Cholinergic Drugs ( parasympathetic drugs ) andexplain them
—- Cholinergic drugs :
1-cholinergic agonist :
1-1: muscranic agonist: they are two
Direct and indirect
- direct action on the receptor : is mean that the drug changing the vital activity of the drug and by that changing the effectiveness of receptors
-indirect action on the receptor: its inhibit Ach Esterase Enzyme which lead to Accumulation of Ach and staminate both M and N receptors
1-2: Nicotinc agonist : they have ganglionic stimulate
2- cholinergic antagonist
explain the prototype of muscuranic Cholinrgic agonist drict act
-Drug : Ach
— mechanisim and Paralogical effect :
1- Cvs M2 : Negative Chomoptropy and Iontropy
2- Blood vessels M3 : vasodilation which lead to hypotension
3- bronchi M3: broncho. construction which will lead to Asthma
3-Eye M3 : contraction of ciliary muscle = meiosis and accumulation of near vision
— chemically : qintryamine thats mean its not passing The BBB and no Side effect of The CNS
— metabolism : by CholinoEstrase
—— no clinical use duo to multiple act
— Side effect :-we can shortcut it in words
» DUMBLES
-D: Diarrhia
-U: Urintation
-M: miosis
-B: Bradycardia + Broncho construction
-L : lacrimation
-E: emesses > vomiting + excitation of the CNS
-S: salivation
-Contra indication : 1- a patient with Bronchial asthma
2- a patient with organic obstruction in the bladder escipchally (bethanechol)
Explain the Mucurunic agonist ( Dirct act )
-Drugs :
1-Carbacol
2- Pilocarpine
—–
-Drug : Carbacol 0.1 % Eyedrops
( direct action on the receptor)
-pharamlogical effect:
1- mechanism : stimulates M , N receptors so isn’t selective
2- its cholinoEstrase so its doesn’t metabolised by True or pesdu so it has long duration
-Action : Miosis > and increase out the flow from canal of schalem so its decrease the intraoccular pressure
— Uses : Use Rarely To treat glycoma and only Eyedrops ( locally ) because it has multiple act by stimulating M,N receptors
- side effect : no side effect because it’s given locally
—-
-Drug :
1- Pilocarpine 1-5% Eyedrops
-( direct action on the receptor)
- mechanism for pilocarpine :stamulate M receptor miosis which lead to open the canal of sechlem and tubercle meahwerk and the Equaceumer goes out so the Iop decreases
-pahrmalogical effect : increace the gland secretion
-Uses to treat : dryness of the body or Suögern syndrome
—-
-contra indecation : 1- a patient with Bronchial asthma
2- a patient with organic obstruction in the bladder
explain the muscrinc Agonist ( indirect act on the receptor) and the drugs and explain them
— indirect act on receptor: its mean its the drug inhibit the AchE enzyme which results in accumulation of ach and stimulation of both M and N receptor
— type of bonds :
1- Reversible : Anticholino Esterase they do Carbomilation of the Enzyme for 2-3 hours
2- Irreversible : anticholino Estrase yheu do phospharlation and they inhibit the AchE for long duration
–Drugs :
1-Neostigmine
2- Donepezil
3-Rivastigmine
4- Galantamine
——-
-Drug : Neostigmine 0,015 T
(indirect act on receptor)
—chemically : its synthatic from the physostigmine, so its quntary amine
so its polar > less absorbed and dont pass BBB ,has only peripheral effect because its cant pass the BBB
- mechanism: inhibit the achE so Ach increase so stimulate N,M receptor
-metabolsie by : anticholino estrase
— uses: usually used for treat
1- Urin retention ( post operation under one condition which there is no organic obstruction)
2- for paralytic , Elus
3-for toxins of non-depolarised drug ( like mevacurium )
4- treat of myasthenia graves
——–
-drug :
1-Donepezil 0,01 Tab
2-galatamine 0,005 tab ,
3-Rivastgmine 0,018 capsule
- mechanism: inhibit achE and increase Ach in the synaptic cleft
-uses : to treat Alzahimar because it can pass the BBB so it has more selectively on the central effect
explain the muscarnic blockers , and the prototype of muscurunic blockers
— they are 2 types
1- natural compounds : Ex Atropin from the planet Atropepladona
2- syntactic from the Atropin
—- general features of natural compounds
1- they are tarshally amine
2- non selective ( blocks M1, M2,M3 )
-Dif of muscranic blockers: its substance which will block or inhibit the muscranic receptor
——–
— Drug: Atropin A 0.1%-1ml
its the prototype of The muscrinc Blockers
-Attopin : has high affinity to muscranic receptors and prevent the receptors to bind with Ach
— chemically : planet alkaloids, tatshally amine , pass BBB
—Kenatics :
1- absorption : good
2- distribution : all the body include CND
3-metabolism: liver
4-excretion : portion metabolise and another unchanged
— mechanasim effects :
1-CVS : by blocking the M2 which located in the atrium it will decrease the heart rate and if it high dose > tachycardia
2-blood vessels : which consist of M3 there is nothing will happen because the B.V is non innervated receptor
3-Respiratory system : the bronchi which consist of M3 : inhibit the bronchi construction and it will cause bronchi dilation, passive effect bcs receptor a1 will take lead
4-GIT and urnary : which consist of M3 if get blocked will lead to relax of the wall and close of the sphincter ( could casue a constapation and urin retention )
- and HCL will decrease
5-Exocrine glands : which consist of M3 blocking of the receptor will lead to dryness of all body and hypothermia
6- Eye :1- cycloplegia passive midrosis
2-dryness of the eye
7- CNS : SAD-HC
—
Side effect :
1- glaucoma
2- tachycardia
3-Constapation + urin retention
4- Dryness
— uses :
- we don’t use all the time the Atropin because it has multiple act so we use it or we use it synthetic derivatives
1- bronchil asthma
2- Dahrria
3-myocardial infraction ( to treat the bradycardia) main use of atropine
4 uncontrolled bladder
explain the synthatic dervative of atropine ( muscranic blockers )
-Drug - Pirenzepine T0.15
-Mechanasim : selctive blocker on GIT M3+M1
-Uses: Colic , Dhirria , HCL ( stomach ulcers )
——
-Drug - Tolterodine T0.001
-Mechanasim : selctive blocker on GIT M3 ( sphencter )
-Uses: Cystits , Urine incontenance
–
-Drug - Tropicamide 0.5% -1ml Eyedrops
-Mechanasim : selctive blocker on Eye M3
-Uses: for fundus examnation of the eye dou to mitosis
—-
-Drug - ipratropium spray 1 dose = 0.00002 for inhaltion
-Mechanasim : selctive blocker on Bronchie M3
-Uses: for bronchil ashtma
—-
-Drug - trihxyphenidyl T 0.002
-Mechanasim : selctive blocker on CNS M1
-Uses: for decreace the prakinsonsim effect
explain the Antinicotonic
—there is 2 types:
1- ganglionic blocker :
2- neuromuscular blocker :
2.1 depolarsid
2.2 non-depolarsie
————-
1- ganglioinc blocker:
-drugs :Trimethaphan A 0.25
-mechanasim: they are compatator blockers for ach at the recptor of both para and sympathatic ganglion
-pharmalogical effect : bcs of the lack of selctivity they are rarly used in clincal agncy
-uses: hypertension
—————————–
2- neuromuscular blocker :
2.1: non depolarised
-drugs : Tubocurarine A 1%-1.5ml
its the prototype and there a drevativis
1-mivacurium. A 2%-5ml
2-Atracurium A 1%-5ml
— all these drugs connot given orally bcs they can pass BBB
- metabolism:
_mivacurium : by pesedu Ach enzyme
_Atracurium : by hydrolysis in plasma
— duration :
- mivacurium : 20min
- Atracurium : 30 min
—-
-mechanism of effect :
compatative block of Ach at the Nm receptors so thats will lead to muscles relaxation by Ach inhibit
—
-to undo the bond we give neostigmine
— adverse effect :
1-skeletal muscles relaxant could devolp into paralysis
2- histamine release so could cause hypotension
3-blood vessels: decrease Bp
——
— uses : skeletal muscles relaxation during operation
——————————
2-1 Depolarised neuromuscular blockers
-drugs : Succinylcholine A 2%-5ml
-mechanism of effect : its consist of 2 phases
-phase 1 : when succinylcholine bind with nicotinic receptor open Na+ channel so lead to depolarization so the muscles contract and the succinylcholine keep bind to receptor and Na+ keeps entering till it reach muscles fatigue
- phase 2 : not necessary to happend in all patient doing the depolarization the muscles dont respond to ach which is temporary paralysis
- pharmacological effect :
1-produce muscles contraction followed by the paralysis
2-release histamine
- therapeutic use : relaxation during surgical operation
- side effect:
1- bradycardia’s
2-muscles pain post op
3-increase bronchi secretion
- Contra indication :
1- hyperkLmia
2-bradycardia
3-hypotension
which concept dose Adroginc receptor is follow , what is the type , location , function of adroginc receptor ?
-Second massager : all the adroginic receptor in the body follow the concept of second massager and they are
> G Protein Linked receptor
————-
1- a1 : follows the Gq second massager
- location :
1-1 Blood vessel’s : V.c
1-2 Uterus : contraction ( but not strong for apportion )
1-3 Eye in the dilator pupil ( radial M.c) : contraction so cause Mydriasis
1-4 GIT & uriniry: in the wall > relaxtion of the wall and contraction of the sphincter
——-
2- a2 : follows the Gq second massager
-Location : they are presynaptic receptor so they located only in the nerves terminal , if they activated they inhibit the Norepinephrine and they called ( selective a2 agonist )
——-
3-B1 : follows the CAMP second massager
-location :
3-1heart > increase all the cardiac properties:
HR,contractility,conductivity,Etc
3-2:Kidney > they are responsible for secretion of Renin
3-3 : Adipocytes
——-
4-B2 : follows the Camp second massager , and its the main roller of fight or flight mode
-location :
4-1:Skeletal muscles :
- facilitate of the nerve muscular transmission
-increase the blood flow by v.d of the blood vessels
-potassium shift : from the blood to the muscles but could cause hypokalmia
4-2:Coronary artery > dilation
4-3: Bronchi > bronchial dilatation
4-4:Liver : gulcogen to glucose
4-5: Eye: regulating the Eye pressure by increase the secretion of Eqousumer
4-6: Uterus > relaxation of the muscles in the Emergency time to prevent apportion
NB! sometime cause Tremors
——
5-B3:follows the Camp second massager
-location : in the adipocytes tissue specifically in the upper part of the body so when its activate cause Lipolysis
in the a1 receptor its always contraction in all the locations but in wall of GIT and urinary is relaxation give the reason?
-bcs first of all the a1 work with Gq second massnger the it will activate Ip3 then ip3 will activate the Ca++ which will activate the Myosin light chain kinase and this how the contraction happens
- but in the wall of GIT and urinray the myosin light chain are absent so the Ca++ open a channel called calcium dependent potassium channel which will cause hyprploarazation duo to the potassium and how the relaxation happens
explain the Prototype of sympathomimetics
-Epinephrine = adrenaline A0.1%-1ml
— its natural in the body located in the
1- nerve terminal
2-Supra renal gland
— Chemistry of Epinephrine:
1- its caticol ring
2- its very sensitive so it can be oxidetis by light and air when its oxidation it become darker in colour and its become toxic called : Adrenochrom
— Phramcokinatiks of Epinephrine:
1- absorption: not orally bcs its water sulable and also in the intestines MAO enzyme which break it down so fast > so only though inhalation or subcouenus
2- destrbuation: goes and distributed all over the body but can pass the BBB bcs its caticol ring
3- metabolism: by MAO enzyme
4- excretion : by 2 forms > -Metanephrine , -Vanlail mandalic acid
— ROA: 1-subcountenous
—-Mechanism of Epinephrine:
- it will stimulate > a1 , a2,b1,b2,b3
NB! the mechanism on a2 its not that effective bcs a2 its parasympathetic
- molecular mechanism : through the 2nd massinger Gq and Camp
—Pharmalogical effect :
1- Heart : it will positive all the heart functions like : chronotropy , inotropy
and if the dose is high > Arethmia and ventricular fibration
2- Blood pressure (Bp) : maximum : 140 systole and 90 dystol , but with Epinephrine :
> systole controlled by cardiac out put
> dystol controlled by peripheral resistance
so it will increase the systole and decrease the dystole in the therapeutic dose
- in the high dose it will increase the dystole bcs the a1 will dominate on B2 which is do V.D so the result V.C
3-bronchi (B2): it will cause broncho dilatation and V.c of the blood vessels in the bronchi which will inhibit the gland from secretion of water and stop the sputum which called :
> broncho decongtion
-4 Eye : decrease the inter ocular pressure by effecting on the cillirly blood by cuseing V.C which will results of decreasing the secretion of the Eqousumer
5- liver : increase the glycolysis so increase the blood glucose
6- hypokalima
—uses :
1-Acute Anephlictic shock :
its type of hypersensitive also called immediate hypersensitive its happened duo to : - Pincillen or - bee bites
- for example : Pencillin hypersensitive your penicillin goes to mast cells and destroy it which is reales the Histamine and histamine will do - sever broncho constraction and sever vasodilation
so treatment by injecting Epinephrine intermsacular in the lateral thigh because the Epinephrine will effect by
- bronchi dilatation
and
- vasoconstriction
2-Acute broncho spasm :its more happens to the kids bcs they had a small airway in the larynx so duo to coughing the larynx wall will get inflammation and edema in the wall of larynx so the airway will get closed and the kid will be hard for him to breath so we give epinephrine to do V.c of the blood vessels of the larynx wall it will decrease the secretion and the edema will disappear and bronchi dilation
3-Cardiac arrest: cardiac arerest means no effective Pules
- so we give Epinephrine Amp through IV so it will result of V.C then we do CPR
4-Local anithtics : for Anastasia with epinephrine so we do vasoconstiction of the blood vessles to stop the blood from washing the anastegic drug
—addvers effect:
1-hypertension
2-cerebral haemorrhage
3-Tremors
4-Tachycardia >Arrhythmia > ventricular fibration
5- Acute heart failure
6- Acute pulmonary Edema( by increasing the heart contractility
——Contra indication :
—- Patient with :
1- hypertension
2-C.V.S diseases
3-high dose
4- cardiac out flow obstruction like: Aortic stenosis
5- Hyper trophic obstruction cardiac Mayobothy : its case in the interventrecular Septum the width of it its normally 12 mm but in the case the Septum with ageing getting thick till reach 17 mm and block the aortic valve , so if we give Epinephrine it will increase the contractility of the heart and the blood will stay in the heart bcs the obstruction
