final exam 1 Smester Q Flashcards
- Types, structure and location of cholinergic receptors. Signal transduction. M-cholinergic
agonists: pharmacological effects, therapeutic application, side effects.
-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
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 (+)
–signal transduction : when the M1-m3 activated THEY ACTEVAT G protein which will actevate Phospholipse c which will actevate the second massgner ( IP3/DAG ) which will cause Calcium influx and cause hyperpolarztion
-about M2 when its acitvated its decrese the CAMP which will decrace the cardiac work
—1— Muscrinc Receptor location and 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)
4-M4: CNS
-2-nectoinc Receptor location and effects :
— 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
-Cholonirgic agonist :
1-1: muscranic agonist: they are two Direct and indirect
–Direct : direct action on the receptor : is mean that the drug changing the vital activity of the drug and bu that changing the effectiveness
-Drug :
1- Pilocarpine 1-5% Eyedrops
2- Cevimeline tablets 30mg for adults
-( 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 :
1- Decrese the COP
2-Decrece bp
3-increace secreatin
4-increace bronchdilator effect
5- increace GIT motality
-Uses to treat : dryness of the body or Suögern syndrome
-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
–indirct : 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
-Drug : Neostigmine 0,015 T
(indirect act on receptor)
- M,N-cholinomimetics (cholinergic agonists). Direct and indirect action. The pharmacological effects, therapeutic application, side effects and contraindications. Principals of organophosphate poisoning treatment. Example of drug prescription
- direct action on the receptor : is mean that the drug changing the vital activity of the drug and bu that changing the effectiveness
-indirect action on the receptor: its inhibit Ach Esterase Enzyme which lead to Accumulation of Ach and staminate both M and N receptors
— Dircet acting drugs :
-Acetylcholine , carbachol , bethanechol
-mechansim : dircet acting drugs they are effecting Ach dirctly on cholinorecptor
-classification :
1- cholinoester : Acetylcholine , carbachol , bethanchol
2- natural ester : Pilocarpine
—Direct acting drugs : Acetylcholine & Bethancholi
-Pharmacological effect :
1-Decrees COP and Bp
2-Increase Bronchial secretion
3-increase GIT motilty
4-Contraction of urinary bladder
-Side effect : Dumbels
-CI :
Heart block , peptic ulcer ,bronchial asthma
————————
-Indirect drugs : there is reversabl and irreversible
1-Reversible: Rivastigmine , Neostigmine Tabs
2-irreversible: Organophsphat
-Mechanism: there is reversible which inhibits the action of anticholinoestrase enzyme which lead to accumulation of The Ach in the synaptic gap / irreversible agents such as organophosphate have the ability to bind to ACHE which lead to accumulation of the Ach in the Synaptic gap and lead to toxicity
—Side effect : Dumbels
-uses : for myathinoa graves , and alzahimer
- M-cholinergic antagonists. Example of drug prescription. The pharmacological effects,
therapeutic application, side effects and contraindications. Principals of atropine overdose
treatment.
— they are 2 types
1- natural compounds alkaloyd : Ex Atropin Amp from the planet Atropepladona
2- sime-synthatic : Ipratropium bromide
—- 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
-—Kenatics :
1- absorption : good
2- distribution : all the body include CND
3-metabolism: liver
4-excretion : portion metabolise and another unchanged
— pharmalogical 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 :
1-bronchil asthma
2-Dahrria
3-myocardial infraction ( to treat the bradycardia)
4-uncontrolled bladder
-CI :
1-Narrow angle glycoma
2-obetrectve diase of GIT
3-hyperplasia
—Atrpoine over dose :
it should be use a cholonirgic agoinst to revers the effect of atropine the most reversable one is physiostigmine
- Drugs affecting the N-cholinergic receptors. Ganglionic blockers. The pharmacological effects, therapeutic application, side effects and contraindications.
18 Drugs affecting the N-cholinergic receptors. Ganglionic blockers. The pharmacological effects,
therapeutic application, side effects and contraindications.
———————–
— 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
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
-CI : hypertintion
- Drugs affecting the N-cholinergic receptors. Muscle relaxants. The pharmacological effects, therapeutic application, side effects and contraindications. Example of drug prescription.
- 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
20 Types, structure and localization of adrenergic receptors. Signal transduction. α-adrenomimetics
(adrenergic agonists): the pharmacological effects, therapeutic application, side effects and
contraindications.
-Second massager : all the adroginic receptor in the body follow the concept of second massager and they are
> G Protein Linked receptor > IP3 > Ca ++++
————-
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
———————————–.
-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
2-IV( only emergency)
3- inhalation
4-intermascular ( best way )
—-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
21 α,β-adrenomimetics (adrenergic agonists): the pharmacological effects, therapeutic application,
side effects and contraindications.
-Drug :Epinephrine A0.1%-1ml
-Drug : Norepinephrine 0.2%-1ml selctive a more then B
-Drug: Isoprenaline 0.5%-1ml slective B more then a
-Drug alpha : phenylephrine a1 ,Clonidine tab , Xylometazoline nasal drops
–they are synthisis and the pathway is : tyrosin is hydrolate into dopa by the effect of tyrosin hydroxlation then dopa is carboxalte into dopamine then to norepinephrine to epinehprine
— 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 By the 2nd massenger of Gq > IP3 / DAG or CAMP
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
22 β-adrenomimetics (adrenergic agonists): the pharmacological effects, therapeutic application,
side effects and contraindications. Example of drug prescription.
- drug : Dobutamine 1%-1ml
- its synthatic and has caticol ring
-mechanism of action : stimulate B1 in the cardiac which lead to increase the cardiac out put - uses or treatment : to treat Cardioginc shock
-Roa: IVi ( intravenous infusion) in salain or glucose
—- - Drug : Salbutamol T 0.0002 , long duration Salmeterol and Formoterol spray 1= 0.00005 , fenoterol T 0.005
- they are synthatic non caticolmine so they could be giving orally and BBB pass
- mechanism of action : stimulate B2
- pharmacological effect :
1- V.D blood vessels of sklatel muscles
2- V.D coronary artery
3- relaxation of uterus
4- glycolysis so increasing blood glucose
5- bronchi dilatation
6- treatment or uses :
— Salmeterol > spray : for bronchial asthma
— fenoterol : for utrine relaxation
—— advers effect : TTT
1- tachycardia
2- tremors
3- tolerance
—C I :
Diabetes. Hypokalemia. Seizures. angina
23 α-adrenergic blockers: the pharmacological effects, therapeutic application, side effects and contraindications. Example of drug prescription.
- they are 3 classes :
1- a1 + a2 non selective blockers
2- a1 selective blocker
3- a2 selective blocker
—————
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
————-
( non-selctive)
—Drug : , Phentolamine tab 0.025
-mechanism: irreversible antagonist at both a1 & a2 its bind covintally with receptor which lead to long blocked of the receptor - pharmacological effect:
1-orthostatic hypotension
2- reflex tachycardia
— uses : to treat Pheochromocytoma but it should be described with B blacker ( Propranolol ) - side effect :
1-orthostatic hypotension
2- impairment of ejection ( male )
3- Meiosis > bcs blocked of a1 in the eye ( redial M.)
———–
(Selective a1 blocker) - Drug : 1- Prazosin 2- Doxazosin longest duration
3-Tamsulosin all Tabs - mechanism: blockes a1 receptor mainly in the blood vessels which lead to V.c and relaxation of smooth muscles of artery and vines
- pharmacological effect :
it cause minimal changes in :
1- renal blood flow
2-Glomerular filtration rate
and improve lipids profile
— uses or treatment:
1- mild or moderate hypertension
2- treatment of congestive heart failure by decreasing the pre load and after load
3- prostatic hyperplasia ( enlarged prostate ) we use Tamsulosin
— adverse effect :
1- first dose hypotension
2- fluid retention
3- false positive test of antinuclear factor of rhemtoid arthritis
4- in female urine incontenance
————
(selective a2 blocker)
-Drug : Yohimbine T 0.025 - mechanism: selective a2 blocker presynaptic in the nerve ending
- phramalogical effect : leads to increase the norepinephrine release
- uses : Used sometimes as Aphrodisiac without clinical evidence
- β - adrenergic blockers: the pharmacological effects, therapeutic application, side effects and contraindications. Example of drug prescription.
- classes :
1- B1+B2 blockers
2- B1 blockers
3- mixed B+a blocker
—- Prototype : Propranolol
——- chemistry:
they are 2 types :
1- lipophilic : B-blocker ex Propranolol can pass to CNS and cleared by haptic metabolism ( first pass metabolism)
2- hydrophilic: B- blocker ex Atenolol have limited penetration to CNS and execrated primarily by kidney with little of hepatic metabolism
— Phramcokintks :
1- absorption: B- blockers are absorbed well after oral administration and many of them have low Bioavailability because of extensive first pass metabolism
— mechanism: blocked B1 + B2 receptor
—Pharmacological effect:
1- C.V.S :
1.1 - Heart (b1) : decrease the cardiac properties
1.2 blood vessels (b2) : prevent the V.D from B receptor in the - coronary artery
-skeletal muscles blood vessels
1.3 Bp : hypotension by > decrease the Cop , Decrease secretion of renin , resting of the baro reflex
2- respiratory : by blocking the B2 in the bronchi the dominant will goes to the parasympathetic which lead to 2.1-B.C
2.2- bronchospasm
3- eye : decrease the IOP duo to blocking the B2 in the epithelium in the ciliary body
4- CNS : anxiety , nightmares , sexual dysfunction
5-skeletal M. : decrease the Essential Tremors
– side effect :
1- fatigue
2- broncho construction
3- Brady cardia or heart block
4- Prephral ischemic
—Uses :
1- hypertension
2- ischemic heart disease ( classic angina )
becs> decrease the myocardial work , increase the systole fling time
, Redistribution of the blood ,
metabolic switch from FFA to glucose
3- Supra ventricular tachy S.V.T :
its disease that is the SA nodes increase the condectellty so by blocking the B1 we decrease the condactellty and increase the refractory period of SA nodes
4-hyper trophic myobothy
5- glaucoma : timolol and betaxolol bcs they are lipophilic
6- pheochromocytoma
—– special effect of B blocker drugs : - Propranolol: has local anesthetic ( inhibit excitability of cardiac muscle)
-Pindolol : its partial antagonist ( so no excessive bradycardia )
-Esmolol : it has very short acting ( so it used during surgical operation for acute hypertension)
-Labetolol : blocks a and B receptor so its good for pheochromocytoma - Carvedilol : antioxidant action
- ## Nebivolol : its the most selective B1 blocker( B blocker non-selective)
- Drug : 1- Propranolol Tab or Amp 2-Timolol Eyedrops
-mechanism: block the B1 and B2 receptor
-pharmacological effect :mentioned in the general description of the B blocker
-uses : 1- hypertension propranolol
2-glucoma Timolol
2- ischemic hear disease ( classic angina )
3-Cardiac S.V.T
4-hyperthyroidism - side effect :
1- broncho construction
2-hypotension
3-bradycardia
4-heart failure
————-
( blocker-selective B1)
-Drug : 1-Metoprolol 2-Bisoprolol
3-Atenolol 4-Betaxolol 5-Nebivolol all tabs
-mechanism: inhibit B1 in heart - uses :
1- anti hypertension
2- anti anginal
— side effect :
1- brandy cardia
2- hypotension
3-heart failure
————
(B+a blocker class mixed antagonist)
—Drug : 1- Carvedilol Tab - mechanism: inhibit b and a1 receptor
- uses: in emergency for acute hypertension
and for pheochromocytoma - side effect : hypotension
- Sedative-hypnotics. Benzodiazepine derivatives: mechanism of action, pharmacological
effects. Differences between barbiturates, benzodiazepines, zolpidem and buspirone. Example of drug prescription.
1-Barbiturates
2-Benzodiazepines
3- Z drugs
4- other drugs
———–
—-Barbiturates
-1-Chemistry :
- all are derivatives from barbituric acid so they are acidic drugs
2- Classification:
2-1 ultra short acting : Thiopental IM
2-2 long action : phenobarbital tab
3-pharmacokinetics:
— all pass BBB and placenta and secreted in the breast milk
4- mechanism of action :
- its dose dependent so :
4-1 normal dose : Allostric modulation of GABA action of GABA - receptor > Enhancement of Cl- conduce > hyperpolarzion > pharmacological effect 4-2 in case of large dose the Barbiturates will compete in the same site of The GABA receptor»_space; and will do the same as before but there be CNS depression
5-pharmacological effect :
5-1 Antianixty effect : in small dose (not much used in this purpose )
5-2 hypnotic effect: in large dose ( and its main use of the drug )
5-3 anaesthetic effect : thiopental drug
5-4 AntiConvaltions effect : phenobarbital
5-5 S.K muscles relaxation
5-6 General CNS depression in large dose including medullary centre
6- uses or treatment:
6-1 phenobarbital: for tonic clonic
6-2 thiopental : for short acting anaesthesia
6-3 promodine used for antiConvaltions
7-treatment of toxicity:
7-1 mechanical ventilator
7-2 iv fluids
————-
—Benzodiazepine
-1-Chemistry :
- all membranes containes fusion of benzen ring with diazepine ring
2- Classification:
2-1 short acting : Midazolam
2-2 intermediate acting : Lorazepam - oxazepam
2-3 long acting : Diazepam - clonazepam
3-pharmacokinetics:
— all pass BBB and placenta and secreted in the breast milk
4- mechanism of action :
4-1 normal dose : Allostric modulation of GABA action of GABA - receptor > Enhancement of Cl- conduce > hyperpolarzion > pharmacological effect 5-pharmacological effect :
5-1 Antianixty effect : in small dose (good results and main use for this perpus)
5-2 hypnotic effect: in large dose
5-3 anaesthetic effect : midazolam
5-4 AntiConvaltions effect : Diazepam - clonazepam
5-5 S.K muscles relaxation
5-6 antergred amnesia
6- uses or treatment:
6-1 Antianxiaty
6-2 insomnia : temazepam
6-3 AntiConvlation: clonazepam
6-4 abscinse seizures : Diazepam
6-5 status epileptics : Diazepam IV
6-6 short surgical operation: midazolam
7-treatment of toxicity:
7-1 drug called : Flumazenil Amp
———-
Z drug
-Drug : Zolpidem Tab 10mg
- mechanism of action : they are structurally different from BZD but they act bu the same mechanism but bind to GABA-A receptor at site close to BDZ
–mechanism : BZD receptor agonist
-pharmacological effect:
1- they are specific hypnotics only
-treatment or uses :
1- to treat insomnia
-adverse effect : risk of dependent and tolerance
- treatment of toxicity:
drug : Flumazenil Amp
——–
-Drug : Buspirone Tab
-mechanism: its 5-HT1A agonist in mid brain
NB! Presynaptic autoreceptors on serotonergic cell bodies in the raphe nuclei , Upon stimulation, these receptors inhibit the firing of 5-HT neurons
-pharmacological effect:
1- selective Antianxiety so no hypnotic effect or Mc relaxation effect
2-its suppress anxiety after long delay 10-14 D
-precaution : don’t mix buspirone with SSRIs it will cause a serotonin syndrome
42 Benzodiazepines: indications for use, side effects. Specific antagonist of benzodiazepines. Example of drug prescription
—Benzodiazepine
-1-Chemistry :
- all membranes containes fusion of benzen ring with diazepine ring
2- Classification:
2-1 short acting : Midazolam
2-2 intermediate acting : Lorazepam - oxazepam
2-3 long acting : Diazepam - clonazepam
3-pharmacokinetics:
— all pass BBB and placenta and secreted in the breast milk
4- mechanism of action :
4-1 normal dose : Allostric modulation of GABA action of GABA - receptor > Enhancement of Cl- conduce > hyperpolarzion > pharmacological effect 5-pharmacological effect :
5-1 Antianixty effect : in small dose (good results and main use for this perpus)
5-2 hypnotic effect: in large dose
5-3 anaesthetic effect : midazolam
5-4 AntiConvaltions effect : Diazepam - clonazepam
5-5 S.K muscles relaxation
5-6 antergred amnesia
6- uses or treatment:
6-1 Antianxiaty
6-2 insomnia : temazepam
6-3 AntiConvlation: clonazepam
6-4 abscinse seizures : Diazepam
6-5 status epileptics : Diazepam IV
6-6 short surgical operation: midazolam
7-treatment of toxicity:
7-1 (antagoinst ) drug called : Flumazenil Amp
-side effect :
1-drawness
2-ataxia
3-Resp Depression
4-tolarance and physical depndens
43 Antiepileptic drugs and mechanisms of action. Drugs for epileptic status. Example of drug prescription.
-classifiction of epilepcy
1- generalized
1-1 Absences seizures
1-2 myoclonic seizures
1-3 tonic clonic
—-
2- focal
2-1 preserved awareness
2-2 impaired awareness
2-3 secondary generalization
—-
NB! if the epilepsy cor more 20 min its called Status epileptics
NB! Fibril seizures occurs in the children when the high fever
—————-
1- first generation :
1-1 phenytoin
1-2 carbamazepine
1-3 Valproate
1-4 ethosuximid
1-5 phenobarbital
1-6 benzodiazepines
——
2- 2nd generation :
2-1 Vigabatrin
2-2 Lamotrigine
—————–
-Drug : Phenytoin tab 0.117
-its first generation drug
-mechanism: inhibit the electrical excitability of neuron by blocking the Na+ channel
( enzyme inducation )
-uses :
1- tonic clonic
—————
-Drug : Carbamazepine tab 0.2
-its first generation drug
-mechanism: inhibit the electrical excitability of neuron by blocking the Na+ channel
( enzyme inducation )
-uses :
1- tonic clonic
2-Focal seizures
———-
-Drug : Valproate tab 0.3
-its first generation drug
-mechanism: mixed mechanism :
1-inhibit the electrical excitability of neuron by blocking the Na+ channel
2-inhibit GABA-t so GABA decrease the neuronal firing
3-block Ca2+ channel
(enzyme inhibt)
-uses :
1- all epileptic seizures but more favorable tonic clonic and myoclonic
———–
-Drug : Ethosuximide tab 0.25
-its first generation drug
-mechanism: block T-type Ca2+ channel in the thalami cortical neurons
-uses : Absence seizures
———-
-Drug :phenobarbital Tab 0.05
-its first generation drug
-mechanism: mixed :
1-Allosteric modulation of Gaba-A receptor
2-Gaba like action ( in large doses)
-uses :
1- tonic clonic
2-Status epileptics
———
-Drug : Diazepam Amp 0.5% -2ml
-its first generation drug
-mechanism: allosteric modulation of GaBa-A receptor
-uses :
1-first line status epileptics
———–
-Drug : Lamotrigine tab 0.5
-its 2nd generation drug
-mechanism: mixed :
1-block Na+ channel
2-decrease the glutamate release
-uses :
1- all type of seizures
-Side effect : steven jhonson syndrome
44 Antiparkinsonic drugs: mechanisms of action. Drugs that cause schizophrenia-like symptoms. Example of drug prescription
- ## its movement disorder characterized by M.s rigidity and tremors and postural instability duo to loss of Dopaminergic neurons in the Sub-statntia nigrea and locus ceruleus resulting in imbalance of Dopaminergic ( inhibitory ) and cholinergic ( excitatory ) influence on the Extrapyramdial systems-1-Dopaminergic drugs :
1-LevoDopa
2-Selegiline
3-Dopamine agonist
4-Amantadine
———-
1-Drug:L-Dopa ( LevoDopa)
—-pharmacokinetics:
-absorbed rapidly from small intestine
-amino acid so drugs like : leucin and isoleucine compete with it - mechanism of action :
Dopamine cant cross BBB but the L-Dope can thats why we give L-dopa then after it pass the BBB the L-Dopa get carboxylated to convert to Dopamine - but to prevent any chance pf carboxylate in the Body tissue we used a drug called Carbidopa which inhibit the carboxylation in peripheral
- and bcs the L-Dopa has short duration of action bcs its metabolise by COMT enzyme so we should give A COMT inhibitor ( Tolcapone or Entacapon )
—Adverse effect :
1-neuasa and vomiting
2-mood changes
3-Dyskinisa
4-on/off phenomenon
——
2-Drug: Selegiline
which is break down the Dopamine
-adverse effect :
1- nausea and vomiting
2- halosanation
3- insomnia
——
3- Drug : Bromocriptine ( dopamine agonists) (schizophrina like action )
-mechanism: its dopamine (D2) agonist differ from L-Dopa in faster and longer duration so it will has no On/off phenomenon
-uses :
1-Parkinsosm
2-hyperprolactimia
3-Acromgly
4- drug Amantadine
-mechanism: its antiviral drug for influenza A2 in the Antiprakonsim the mechanism is unclear but maybe duo to increase Dopamine release and decreasing the reuptake
-adverse effect :
1-nausea and vomiting
2-skin pigmentations
3-hallosantion and mood changes
45 Types of opioid receptors. Classification of opioid analgesics. The mechanism of action of tramadol. Prescribe tramadol.
-DF: drug that relieve or decrease the pain sensation
— Classification:
1- Full agonist:
1-1 Morphine amp
1-2 Fentanyl amp
1-3 Trimeperidine
1-4 Codeine tab
—
2-Partial agonist-antagonist
2-1Buprenorphine
2-2 pentazocine
—
3-analgesics mixed mechanism of action :
3-1 Tramadol Amp
—
4-full antagonist:
4-1 naloxone amp
4-2 naltrexone tab
————
-Endogenous ligand : are ligands found naturally in the body and they are 3:
1-Endorphins = muo , delta receptors
2-enkephalins = muo , delta receptors
3-Dynorphins = kaba receptor
——
- receptors and there effect when they are triggered :
1- Muo : analgesic, Rc depression,Euphoria,meiosis,sedation,
suppression of Gi motility , addiction , bradycardia
2-delta : Rc depression, suppression of Gi motility
3- kaba : dysphoria , meiosis,sedation, suppression of Gi motility,addiction
——
1- molecular mechanism:
-opiate receptor stimulation > Gi > inhibit of adenylate cyclase (AC) > decrease the cAMP which inactivation of Ca2 and activate Channel K+ which lead to Hyperpolaraization
2-mechanism of Spinal analgesia
-the receptor m,d,k located in the post horn of the spinal cord so when the drug enter and stimulate these receptors it’s decreasing the SGR ( substnsia of gluntosa of Rolando ) and decrease glutamate which lead to Disinhibition of the descending Anti-nociceptive pathway
3-mechanism of Supraspinal analgesia
the opeite receptor also located in the brain when it’s stimulate they lead to activate the Descending inhibitory pain control which lead to inhibit the of the sensation comes from the spinal
4- NA mechanism :
also these drugs are responsible for decreasing the NA release which lead to decrease the emotional pain
( ex tramadol )
