INTRODUCTION TO SCIENTIFIC RESEARCH

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LOCAL ANESTHETICS
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Local Anesthetics
Historically the first local anesthetic
discovered was the tropane alkaloid cocaine
Cocaine is still used in ocular surgery
(anesthetic) and nasal/sinus surgery to decrease
post-operative bleeding due to its
vasoconstrictive properties-----cocaine
addicts Readily absorbed from the mucous
membranes with good local activity - Rapidly
hydrolyzed and inactivated due to the presence of
two ester groups Addiction includes both physical
and psychological addiction
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Desirable Properties of Local Anesthetics 1)
Reversible 2) Non-irritating to the tissues
3) Rapid onset of acting 4) Long duration of
acting 5) High therapeutic index 6)
Effective topically and by injection 7) Proper
physical properties (water solubility and
stability in solution)
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LOCAL ANESTHETICS

• CHEMISTRY
• It composed of hydrophilic domain
• Which either tertiary or secondary amine
• and hydrophobic domain
• it aromatic residue
• separated by alkyl chain
• The hydrophobic hydrophilic domains linked
  with either ester or amide
• This bonds determine the pharmacology of L.A.

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ANESTHETICS
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Pharmacological Classes of Local anesthetic a-
Amide 1- Lidocaine (lignocaine) Risk B C 2-
Prilocaine Risk B C 3- Bupivacaine
(Marcain) Risk C 4- Ropivacaine (Naropin) Risk
C 5- Dibucaine Risk C 6- Mepivacaine (
Scandonest or Carbocaine) Risk C 7- Etidocaine
(Dranest) Risk B
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Pharmacological Classes of Local anesthetic B-
Ester 1- Tetracaine (Amethocaine) Risk C 2-
Benzocaine Risk C 3- Cocaine Risk C X 4-
Proparacaine (Fluoracaine) Risk C 5- Procaine
Risk C 6- Chloroprocaine Risk C
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Pharmacological Classes of Local anesthetic C-
Miscellaneous 1- Dyclonine (ketone) Risk
C 2- Pramoxine (ether)
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MECHANISM OF ACTION

• Block initiation propagation of action
  potential
• By preventing the voltage-Dependent increase
  in sodium conduction
• Via physical plugging the transmembrane pore
• The binding site is in the inner end of sodium
  channel

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SEQUENCE OF EVENTS WHICH RESULT IN CONDUCTION
BLOCKADE
1. Diffusion of the base form across the across
the nerve sheath and nerve membrane 2.
Re-equilibration between the base and cationic
forms in the axoplasm 3. Penetration of the
cation into and attachment to a receptor site
within the sodium channel. 4. Blockade of the
sodium channel
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SEQUENCE OF EVENTS WHICH RESULT IN CONDUCTION
BLOCKADE
5. Inhibition of sodium conduction 6. Decrease in
the rate and degree of the depolarization phase
of the action potential 7. Failure to achieve the
threshold potential 8. Lack of development of a
propagated action potential 9. Blockade of
impulse conduction
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CONDUCTION OF A NERVE IMPULSE
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Ionized
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Common features of Local Anesthetics

• Weak bases (pKa gt 7.4) poorly water soluble
• Packaged as an acidic hydrochloride pH 4-7 now
  soluble
• In solution- non-ionized lipid soluble (free
  base) AND ionized water soluble (cation)
• Body buffers raise the pH, increase free base
• lipid soluble form crosses axonal membrane
• water soluble form blocks sodium channel

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Important Clinical Properties of Local Anesthetics

• ONSET
• POTENCY
• DURATION OF ACTION

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Important Clinical Properties of Local Anesthetics

• ONSET pKa
• pKa pH at which 50 of drug is ionized
• LAs lt50 exists in the lipid soluble nonionized
  form
• Only the nonionized form crosses into the nerve
  cell

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ROLE of pH and pKa in LOCAL ANESTHETICS
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Important Clinical Properties of Local Anesthetics

• Speed of Onset
• low pKa fast onset
• Bupivacaine 8.1Lidocaine 7.7
• ? LA action in septic tissue
• acid tissue -gt é ionized of LA-gt slow entry
  into membrane -gt low concentration of LA for
  block

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Important Clinical Properties of Local Anesthetics

• Anesthetic Potency
• Potency ltgt lipid solubility
• Higher solubility ltgt can use a lower
  concentration and reduce potential for toxicity
  LA

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Important Clinical Properties of Local Anesthetics

• DURATION OF ACTION
• Duration ltgt protein binding
• Bupivacaine 95
• Lidocaine 65
• Procaine 6

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Important Clinical Properties of Local Anesthetics

• CLEARANCE
• ESTERShydrolysis via pseudocholinesterase
• AMIDESmetabolism via hepatic enzymes

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Important Clinical Properties of Local Anesthetics

• Absorption of local at site
• LAs cause some vasodilitation
• LA washout related to blood flow
• LA toxicity related to rate of absorption via
  blood flow

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Important Clinical Properties of LAs

• ADDITION of VASOCONSTRICTORS
• 1- Why it is combined with L.A. ?
• Vasoconstriction ltgt slows systemic absorption
  increases duration
• 2- Epinephrine is commonly used in 1 in 200000 to
  80000 (5ug-12.5ug/ml)
• Least effective with high lipid soluble LAs
  (bupivacaine/etidocaine)
• Epi may produce distal and systemic effects

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• ADDITION of VASOCONSTRICTORS
• 3- The total dose should not exceed 200-500ug
• 4- Epi-Drugs interaction
• Tricyclic anti-depressant
• Sympatholytic drugs
• 5- Contraindications ?
• not recommend for digits injection
• 6- Do you prefere Norepinephrine OR EPINEPHRINE?

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Effect of pH on the efficacy of local
anesthetics 1- The activity of local anesthetic
is strongly pH dependent 2- L.A. need to
penetrate the nerve sheath and axon to reach the
binding site of sodium channel 3- In acidic
media penetration is very poor 7- Inflammed
infected tissues are acidic
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• ADDITION of Sodium Bicarbonate
• NaHCO3 - é pH nonionized base
• Speeds onset of block
• 1 mEq NaHCO3 per 10 ml Lido/Mepiv
• .1 mEq NaHCO3 per 10 ml Bupiv

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Methods of administration of L.A. 1-
Infilteration Lidocaine or Bupivacaine 2-
Surface Lidocaine, tetracaine,
benzocaine 3- Intravenous regional anesthesia
mainly lidocaine , prilocaine 4- Nerve block
lidocaine or bupivacaine 5- Spinal
anesthesia mainly lidocaine , tetracaine 6-
Epidural anesthesia mainly lidocaine , marcain
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A. Surface or Topical Anesthesia 1. The oral
cavity, pharynx, larynx and tracheobronchial tree
provide examples of mucosal surfaces where local
anesthetics are applied topically. 2. A great
danger exists in these areas for overdosage since
rapid absorption into the circulatory system may
occur and exceed the rate of detoxification of
the drug. 3. To avoid this danger use a fine
spray with a low concentration of the drug and
limit the volume of solution used. 4. Most
often used agents cocaine (4-10), tetracaine
(1-2) and lidocaine (2-4) B. Local
Infiltration 1. Used for superficial surgery
such as removal of moles, warts, sebaceous cysts,
etc. Also for iv insertion. 2. Use the
lowest concentration of drug which will block
sensory perception. Large volumes are generally
used. 3. Epinephrine approximately doubles
duration of action. 4. Most frequently used
agents include lidocaine 0.5-1 and Bupivacaine
0.5
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C. Regional Nerve Block and Field Block 1.
Field block Similar to local infiltration, but
the goal is to specifically interrupt nerve
transmission proximal to the site to be
anesthetized. 2. Nerve Block - The goal is to
inject local anesthetic into or about individual
nerves or nerve plexuses. Produces even greater
areas distal of anesthesia with a smaller amount
of drug 8. Agents include Procaine
(0.5-2.0) Lidocaine (1-2) Mepivacaine (up to
7 mg/kg of 1-3) Bupivacaine (0.25-0.75 up to 3
mg/kg ) Tetracatine (up to 1.5 mg/kg of
0.1-0.2).
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D. Intravenous Regional Anesthesia 1.
Consists of iv injection of local anesthetic into
vein of exsanquinated extremity with proximal
tourniquet. 2. Binding of drug occurs in
tissues of extremity - with tourniquet down
(after 15-30 min minimum up time) only 15-30
released into systemic circulation. 3. More
effective in upper extremity 4. Lidocaine
(1.5 mg/kg of 0.5) frequently used.
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E. Epidural Anesthesia (caudal anesthesia) 1.
Epidural space terminates cephically at the
foramen magnum. 2. Epidural anesthesia
consists of epidural injection into the lumbar,
or less frequently, the thoracic area. 3. Two
sites of action (a) diffusion into subarachnoid
space (b) diffusion into paravertebral area
through intervertebral foramina to produce
multiple paravertebral blocks
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Continue--. Epidural Anesthesia (caudal
anesthesia) 4. Danger of inadvertent subdural
and subarachnoid puncture. Lidocaine
Bupivacaine for longer action are used. 5.
Unlike spinal, no differential zone of
sympathetic blockade. There is a zone of
differential motor blockade 4-5 segments less
than sensory block. 6. Other dangers include
anterior spinal artery syndrome, hematoma,
infection, and adhesions. 10. Advantages
include (a) blood pressure remains stable (b)
in obstetrical cases, the mother retains motor
control of the abdominal muscles and can assist
in the delivery of the fetus
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F. Spinal Anesthesia (subarachnoid block) 1.
Injection of local anesthetic into the lumbar
subarachnoid space usually at T2-T3 or T3-T4
interspace. 2. Distribution of the drug in the
subarachnoid space determines the level of
anesthesia. This is controlled by a)
Positioning of the patient b) Speed of
injection c) Specific gravity of solution
d) Volume injected 3. Nerve fibers
affected in the following sequence autonomic
? sensory ? motor 4. Zones of differential
anesthesia sympathetic block segments higher
than sensory - motor segments lower
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Continue-- Spinal Anesthesia (subarachnoid
block) 5. It causes sympathetic blockade. Most
important changes are on venous side of
circulation. 6. Cardiovascular effects
hypotension, bradycardia, ?preload ?afterload
7. Respiratory complications due to ischemic
paralysis of medulla and not usually phrenic
paralysis 8. Other dangers chemical
transection of cord traumatic
destruction of a spinal end artery
traumatic damage of a nerve root chronic
arachnoiditis postural headache and
infection. 9. Agents frequently employed
include Tetracaine Lidocaine
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Pharmacology of L.A.

• They interfere with function of all organs in
  conduction occurs
• A- CNS
• Stimulate CNS leads to restlessness and may
  proceed by clonic convulsion
• Then CNS depression
• Respiratory failure is main cause of death
• Drowsiness is the most complain

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Pharmacology of L.A.

• B- Cardiovascular
• Decrease mycardium excitability
• Conduction
• Decrease force of contraction
• Hypotension
• These effects occurred in high dose which cause
  CNS toxicities
• Arteriodilation
• Rarely occurs in infilteration

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Pharmacology of L.A.

• C- Hypersensitivity
• Mostly occurred with ester type
• Allergic dermatitis
• asthmatic attack
• Amide almost free of hypersensitivity

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Lidocaine 2 1- DOSE OVER 10 YRS Not exceed
6.6 mg/kg or 300 mg per dental appointment 2-
under 10 years 100-150 mg per dental
appointment 3- Drug interaction -beta
blockers -antiarrhythmia agents 4- Metabolism

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• Prilocaine 4
• 1- DOSE
• Less than 10 yrs 40 mg per setting or less
• greater than 10 yrs and adult 40-80 mg
• Not exceed 400-600 mg in adult
• 1- Toxicities
• Methemoglobinemia
• 2- under 10 years 100-150 mg per dental
  appointment

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• BUPIVACAINE 0.5
• 1- DOSE
• Less than 10 yrs NOT ESTABLISHED
• greater than 10 yrs and adult 9 mg
• Not exceed 90 mg in adult per dental appointment
• 2- duration
• Nerve block 5-7 hrs
• 3- Toxicities
• - much greater than lidocaine

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MEPIVACAINE
Amide Products Longer duration of action
1- Indications Peripheral, transvaginal,
paracervical, caudal, epidural and infiltration
nerve block, dental procedures 2- protein bound
78 3- Warnings NOT recommended for
obstetrical epidural anesthesia due to cardiac
arrest and death Reserve the 0.75 solution
for surgical procedures where prolonged activity
is neededdanger of inadvertent IV injection and
cardiac arrest
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ETIDOCAINE
Amide Products - Longer duration of action
1- Indications peripheral, central or lumbar
peridural nerve block intra-abdominal/pelvic/lowe
r limb/ceasarean section surgery caudal or
maxillary block 2- Onset of action 3-5 minutes 3-
with a duration of action of 5-10 hours 4-
surprisingly epinephrine addition does NOT
increase the durationwhy?----Partition
coefficient is 7050X of procaine---94 protein
bound
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ROPIVACAINE
Amide Products - Longer duration of action
1- Indications local or regional anesthesia for
surgery, post-operative pain management and
obstetrical procedures 2- Avoid rapid
administration of large doses---use fractional or
incremental administration 3- ideal for
continuous infusion for epidurals during birth 4-
Onset of action is 10-15 minutes 5- with a
duration of action of 2-8 hours---safe to use
this as an epidural product for up to 24 hours
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TETRACAINE
Ester Products
1- Indications Spinal anesthesia including
high, median, low and saddle blocks including
prolonged action of 2-3 hours 2- Slower onset of
action than procaine but duration is 2-3 hours
------ can increase to 3-5 hours by including
epinephrine 3- This drug should not be used in
children due to a lack of safety data
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COCAINE (1)- Mechanism of action A- Blocks
sodium channel B- inhibit NE UPTAKE-1 (2)
Direct vasoconstrictor action and potentiation
sympathetic system (3) Extensive
cardiovascular actions (4) Powerful CNS
stimulant (5) Considered a narcotic with
potentially for psychic dependence (6) Used for
surface anesthesia in 1.0-10.0 solutions,
occasionally with epinephrine (7)
Metabolized by esterases and hepatic enzymatic
degradation t1/2 after oral or nasal
administration, approximately 1 hour

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LOCALLY ACTING AGENTS
LOCAL HAEMOSTATIC AGENTS
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LOCALLY ACTING AGENTS
LOCAL HAEMOSTATIC AGENTS

• 1- Sympathomimetic
• Epinephrine with LA
• Epinephrine-imprignated cord to retract and
  control gingival haemorrhage
• 2- Astringents STYPTICS
• They react with proteins of oral cavity and make
  protective layer
• Aluminum chloride (Sansilla)
• Example of Styptics Silver nitrate rod

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LOCAL HAEMOSTATICS

• Aluminum chloride retraction cord (HEMODENT 25)
• Tannins Pyralvex
• it is an oral paint contains tannic acid and
  salicylic acid
• - It is used for mild peri-oral lesion less
  effective in oral lesion
• 3- Mechanical haemostatics
• They forms matrices in which blood cells and
  fibrin can trapped
• They are more effective than astringent, styptics
  or sympathomimetics
• in controlling capillary oozing surface
  bleeding

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Types of mechanical haemostatics

• 1- Absorbable gelatin (Gel Foam)
• Advantages of absorbable gelatin
• It does not interfere with the followings
• Thrombin
• Epithelization
• Bone regeneration
• 2- Oxidized cellulose (Oxycel Novocel)
• It has high affinity to haemoglobin it is form
  of gauze of cotton pellets
• It is more effective than Gelfoam
• It interfere with followings
• - Epithelization bone regeneration (not
  suitable for packing in bone fracture
• Inactivates thrombin

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• 3- Oxidized regenerated cellulose (Surgicel)
• Advantages
• - It does not interfere with epithelization
• -Therefore , it is suitable for surface dressing
• Disadvantages
• - It interferes with bone regeneration
• - Inactivates thrombin
• 3- Microfibrillar collagen hemostat (Avitene)
• It is in the form of powder used to control
  bleeding after oral surgery
• Advantages
• - It does not interfere with
• epithelization
• bone regeneration
• activity of thrombin
• Disadvantage it is source of animals which may
  transfere diseases

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SYSTEMIC HAEMOSTATICS

• HAEMOSTATIC SYSTEMS
• 1- Formation of fibrin via clotting factors
• 2- Fibrinolysis
• 3- Platelets aggregation
• 4- Blood vessels (PGE12)

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Examples of systemic haemostatic agents

• VITAMIN K
• Role of vitamin K in clotting system
• - Vit K is necessarly for final stage of
  clotting factors synthesis such as prothrombin
  ,factor vii, ix x
• Premature Mature clotting factor
• Clotting factors

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• CAUSES OF VIT K DEFICIENCY
• 1- Obstructive jaundice
• 2- malabsorption
• 3- Reduced GIT flora
• -Rarely after broad spectrum antibiotics
• CLINICAL USES OF VITK
• 1-Reverse bleeding induced by oral anti-coagulant
• 2- Inadequate vit k availability
• 3- new born baby

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• VIT K Preparations
• vit k1 (phytomenandione) konakion
• - it is lipid soluble and injected in new born
  baby
• onset within 12 hours
• Menadiol sodium phosphate (vitk3)
• it is water soluble
• onset 24 hrs
• prefered in malabsorption or obstructive
  jaundice
• It has tendency to induce hemolytic anemia

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TRANEXAMIC ACID

• 1- MECHANISM OF ACTION
• Prevents plasminogen not to attach to fibrin
• resulting in inhibition fibrinolysis
• inhibits the proteolytic activity of plasmin
• 2- Clinical uses
• Use as Mouthrinse 4.8 to prevent bleeding in
  hemophiliac patient under warfarin due to
  dental extraction
• ORAL 25 MG/KG FOR 2-8 DAY in haemophiliac
• Hereditary angioedema menorrhagia
• Thrombolytic over dose

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TRANEXAMIC ACID

• 3- pregnancy Risk factor B
• to prevent bleeding in hemophiliac patient
  under warfarin due to dental extraction
• 3- Adverse effects
• If taken orally
• GIT Disturbances such as diarrhea
• Hypotension
• Thrombosis
• Blurred vision requires regular eye examination
• -Regular liver function tests in long term oral
  use for hereditary angioedema

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AMINOCAPROIC ACID

• 1- Mechanism of action
• Inhibits the activation of plasminogen to plasmin
• 2- Clinical uses
• Treatment of excessive bleeding from fibrinolysis
• 5-30 g/day in divided dose at 3-6 hrs interval

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AMINOCAPROIC ACID

• 3- pregnancy Risk factor C
• 4- Adverse effects
• Hypotension
• bradycardia
• Arrhythmia
• Myopathy
• GIT irritation

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APRPTONIN (Trasylol)

• It is inhibitor of plasmin (plasmin causes fibrin
  lysis)
• CLINICAL USES
• - Over dose of thrombolytic drugs such
  streptokinase
• - Hyperplasminia as a result of mobilization
  and dissection of malignant tumor
• SIDE EFFECTS
• Hypersensitivity
• -localized thrombophlebitis

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ETHAMSYLATE OR ETAMSYLATE DICYNENE

• 1- Mechanism of action
• CORRECT ABNORMAL PLATELETS ADHESION
• 2- Clinical uses
• Short term use in blood loss in menorrhagia(500mg
  tablets four times daily during menses
• Prophylaxis and treatment of periventricular
  haemorrhage in low birth weight infants (i.v. or
  i.m.)
• 3- Clinical uses
• - Rashes , Nausea and Headache

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DESMOPRESSIN ACETATE(Stimate)

• 1- Mechanism of action
• Enhance reabsorption of water in kidney
• Increase Von Willebrand factor factor viii
• 2- Clinical uses
• Control bleeding in mild hemophilia Von
  Willebrand disease during dental extraction
• Diabetes insipidus
• Nocturnal enuresis
• CAUTION Avoid overhydration (it has ADH
  activity)

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DESMOPRESSIN ACETATE

• 3- pregnancy Risk factor B
• 4- Adverse effects
• Facial flushing
• Dizziness
• Nasal congestion
• hyponatremia
• Water intoxication

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BLOOD PRODUCTS

• 1- Anti-hemophilic factor (Kogenate)
• It is factor viii derived from recombinant DNA
• - CLINICAL USES
• - Control bleeding in hemophilia A
• - Life threatening haemorrhage
• 2- FACTOR VIIa (NovoSeven)
• It is recombinant DNA
• CLINICAL USES
• PATIENT WITH INHIBITORS TO FACTORS VIII IX

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BLOOD PRODUCTS

• 3- FACTOR IX (Replenine)
• - CLINICAL USES
• - it indicated in patient with factor ix
  deficiency (Hemophilia B)
• - CAUTION Risk for thrombosis

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FIBRIN GLUE (Beriplast)

• 1- Composition
• Two separate solutions
• a- fibrinogen
• b- thrombin calcium
• It is completely reabsorb within 2 4 weeks
• Some products contain
• tranexamic acid or aprotonin
• 2- Effective in preventing bleeding in bleeding
  disorders

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• Management of patient under warfarin

• 1- Minor surgery
• Use tranexamic mouth rinse
• without adjustment of anticoagulation if INR is
  less than 4
• 2- Major surgery
• Stop warfarin preoperative
• use low molecular weight heparin

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Intrinsic Pathway
Extrinsic Pathway
Tissue Injury
Blood Vessel Injury
Tissue Factor
XIIa
XII
Thromboplastin
XIa
XI
IXa
IX
VIIa
VII
Xa
X
X
Prothrombin
Thrombin
Factors affected By Heparin
Fribrin monomer
Fibrinogen
Fibrin polymer
Vit. K dependent Factors Affected by Oral
Anticoagulants
XIII
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• ANTI-COAGULANTS

• 1- Drugs inhibit vit k actions (oral
  anticoagulant)
• By prevents maturation of the clotting factors
• slow onset (3 days)
• 2- Drugs directly acting on the clotting factors
• - Rapid onset (Heparin)
• 3- Drugs inhibit platelets aggregation
• 4- Fibrinolytic drugs (dissolve clot)

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• ORAL ANTI-COAGULANTS
• WARFARIN (Coumadin)

• 1- CLINICAL USES OF WARFARIN
• Prophylaxis and treatment of venous thrombosis
  such as
• - Deep vein thrombosis (DVT)
• - Atrial fibrillation
• - prosthetic cardiac valves with
  antiplatelets
• - thromboembolic disorders such post MI or
  Stroke and embolism

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• ORAL ANTI-COAGULANTS
• WARFARIN (Coumadin)

• 2- MOA OF WARFARIN
• Warfarin interferes with hepatic synthesis of vit
  K-dependent factors (ii, vii, ix, x)
• PREVENT RECYCLING OF VIT K by inhibiting
  reductase enzyme which convert epoxide vit K to
  vit K
• 3- ONSET OF WARFARIN
• Within 36-72 hours

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Mechanism of action
Descarboxy Prothrombin
Prothrombin
Reduced Vitamin K
Oxidized Vitamin K
NADH
NAD
WARFARIN
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• ORAL ANTI-COAGULANTS
• WARFARIN (Coumadin)

• 4- MONITORING ITS EFFICACY
• Prothrombin time expressed by
• International Normalized Ratio (INR) determined
  daily initially then at longer intervals depends
  on the response
• INR 2-2.5 For prophylaxis of DVT, AF,
  Cardioversion, dilated cardiomyopathy, MI,
  Rheumatic valve disease
• INR 3.5 For recurrent DVT , pulmonary embolism
  and mechanical prosthetic heart valve

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• ORAL ANTI-COAGULANTS
• WARFARIN (Coumadin)

• 4- ADVERSE EFFECTS OF WARFARIN
• The main is hemorrhage
• Skin necrosis in patient with protein c s
  deficiency
• 5- PREGNANCY
• AVOID RISK FACTOR D
• REPLACED BY HEPARIN

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• ORAL ANTI-COAGULANTS
• WARFARIN (Coumadin)

• 6- DRUG INTERACTION
• INCREASE EFFECTS
• - NSAIDs
• - Sulfa drugs
• - cimetidine
• Decrease effects
• liver enzyme inducer such as
• -phenobarbitone, rifampicin, phenytoin

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• HEPARIN

• 1- RAPID ONSET, inject only S.C. OR I.V.
• 2- CLINICAL USES
• Preventive and treatment of thromboembolic
  disorders such as DVT, MI, pulmonary emobolism
• patient undergoin general surgery (low dose)
• orthopedic surgery
• unstable angina Pregnancy
• Extracorporeal circuits such as hemodialysis
  cardiopulmonary bypass

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• HEPARIN

• 3- DOSES OF HEPARIN
• PROPHYLAXIS DOSE
• A- Post-operative MI 5000 units s.c. every
  8-12 hrs
• B- pre-surgery 5000 units 2 hours before surgery
• C- Pregnancy 5000 -10,000 units every 12 hours
  (REQUIRED APTT monitoring

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• HEPARIN

• 4- MECHANISM OF ACTION OF HEPARIN
• Heparin enhances the activity of anti-thrombin
• It inhibits factor X in small dose
• 5- MONITOR THE EFFICACY
• Prophylaxis dose does NOT require
• APTT (Activated partial thromboplastin)
• APTT should be in the ranges 1.5-2.5

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Heparin mechanism of action
Heparin
Antithrombin III
Thrombin
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• HEPARIN

• 6- ADVERSE EFFECTS
• Bleeding if APTT more than 3 or
• - impaired hepatic or renal functions
• Thrombocytopenia
• Osteoporosis (long term use)
• skin necrosis hypersensitivity
• It may induce hyperkalemia by inhibition of
  aldosterone secretion
• 7- ANTIDOTE OF HEPARIN
• - Protamine sulfate 100mg neutralizes 100 unit

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• LOW MOELCULAR WEIGHT
• HEPARIN

• 1- EXAMPLES
• Enoxaprin , Dalteparin Ardeparin
• 2- Advantages
• A- Do not required APTT monitoring
• B- because it has little effects on antithrombin
  but it potent inhibition on factor Xa
• C- Long duration (once daily)??? ???

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• HEPARINOID

• 1- EXAMPLES
• DANAPAROID
• 2- MOA inhibits Xa IIa factors
• 3- Advantages
• A- Low incidence of thrombocytopenia
• therefore it can be used in patient had
  history of thrombocytopenia due to heparin
• 4- Disadvantage not effectively antagonized by
  protamine sulfate

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• ANTIPLATELETS AGGREGATION

• 1- EXAMPLES
• Aspirin
• Clopidogrel
• Dipyridamole
• Ticlopidine
• Abciximab
• Eptifibatide
• Tirofiban

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• ANTIPLATELETS AGGREGATION

• 2- THEY DECREASE PLATELETS AGGREGATION and
  inhibit thrombus formation in the arterial
  circulation where anti-coagulants have little
  effects.
• 3- General Clinical uses
• cerebral vascular diseases such as Transient
  ischemic attack (TIA)
• Unstable angina
• Post MI
• Coronary artery bypass surgery Angioplasty

88

• ASPIRIN

• 1- CLINICAL USES OF ASPIRIN (small dose)
• Prophylaxis for MI (75mg- 81mg-160-325 mg)
• Transient ischemic episode stroke (600 mg
  twice daily)
• Following coronary bypass surgery
• percutaneous transluminal coronary angioplasty
• Eclampsia in small dose ? Unlabelled
• 2- MOA Irreversibly inhibits COX
  (cyclooxygenase) leading to inhibit thrombane A2
  in platelets

89

• ASPIRIN

• 3- ADVERSE EFFECTS OF ASPIRIN
• GIT upset may develop ulcer
• May precipitate bronchial asthma in patient has
  histry of bronchial asthma
• Some patient develop subcutaneous hemorrhage (as
  spots)
• 4- contraindication
• children under 12 years and breast feeding
  mother
• active peptic ulcer
• bleeding disorders
• 5- Caution
• asthma , pregnancy

90

• CLOPIDOGREL (PLAVIX)

• 1- CLINICAL USES
• Reduces atherosclerosis events such as MI,
  Stroke peripheral artery diseases
• Prevent of thrombotic complications after
  coronary stenting
• Acute coronary syndrome such as unstable angina
  or non-Q-wave MI
• It can be used instead of aspirin if patient
  allergic to aspirin
• 2- MOA
• It blocks the ADP receptors in platelets which
  prevent fibrinogen binding to platelets leading
  to reduce platelets aggregation.

91

• CLOPIDOGREL (PLAVIX)

• 3- ADVERSE EFFECTS
• Bleeding (GIT Brain) leukopenia
• GIT upset such as gastritis (less than aspirin)
• 4- CONTRAINDICATIONS
• Active bleeding avoid first few days after MI 7
  days after stroke
• Not recommend for angioplasty
• Stop it 7 days before surgery
• Liver impairment
• Breast feeding

92

• TICLOPIDINE (TICLID)

• 1- CLINICAL USES
• It is reserved for patients who are intolerant to
  ASPIRIN
• Prophylaxis of major ischemic events in patient
  with a history of ischemic stroke
• Adjuvant therapy with aspirin following coronary
  stent to reduce stent thrombosis
• 2- MOA
• Similar to plavix

93

• TICLOPIDINE (TICLID)

• 3- ADVERSE EFFECTS
• Bleeding
• Neutropenia , agranulocytosis pancytopenia
• Thrombotic thrombocytopenic purpura
• Increases liver enzymes
• Jaundice
• hyperlipidemia

94

• DIPYRIMADOLE (PERSANTIN)

• 1- CLINICAL USES Maintains patency after
  surgical grafting include coronary artery bypass
• Used with Warfarin to decrease thrombosis in
  patient after artificial heart valve replacement
• Use with ASPIRIN to prevent thromboembolic
  disorders
• It can be given 2 days prior open heart surgery
• 2- MOA Inhibits adenosine deaminase
  phosphodiesterase leading to accumulation of
• Adenosine , adenosine nucleotides These inhibit
  platelets aggregation
• cAMP this causes vasodilation

95

• DIPYRIMADOLE (PERSANTIN)

• 3- ADVERSE EFFECTS
• Hypotension
• Headache
• Increased bleeding during or after surgery
• Worsening symptoms of coronary heart disease
• 4- CAUTIONS
• Rapidly worsening angina
• Aortic stenosis
• Recent MI
• CHF Migraine

96

• ABCIXIMAB(REOPRO)

• 1- CLINICAL USES
• Adjunct to percutaneous transluminal coronary
  angioplast
• Prevention of acute ischemic complications in
  patients at high risk for abrupt closure of
  treated coronary vessels
• Use with heparin in unstable angina
• 2- MOA
• It binds with platelets iib/iiia receptors
  preventing their aggregation

97

• FIBRINOLYTIC DRUGS

• 1- EXAMPLES
• Alteplase (recombinant DNA tissues plasminogen
  activator)
• Reteplase
• Streptokinase
• tenecteplase

98

• ALTEPLASE (ACTIVASE)

• 1- CLINICAL USES
• Management of acute MI
• pulmonary embolism for lysis of thrombi
• 2- MOA
• It initiates local fibrinolysis by binding to
  fibrin in clot and converts entrapped plasminogen
  to plasmin

99

• ALTEPLASE (ACTIVASE)

• 3- adverse effects
• Multiple emboli
• Arrhythmia due to cardiac reperfusion
• bleeding

100
ANTICOAGULANT DRUGS TO TREAT THROMBOEMBOLISM
Drug Class Prototype Action Effect
Anticoagulant Parenteral
Heparin
Inactivation of clotting Factors
Prevent venous Thrombosis
Anticoagulant Oral
Warfarin
Decrease synthesis of Clotting factors
Prevent venous Thrombosis
Prevent arterial Thrombosis
Antiplatelet drugs
Aspirin
Decrease platelet aggregation
Breakdown of thrombi
Thrombolytic Drugs
Streptokinase
Fibinolysis
101

• ORAL PROTECTIVE AGENTS

• 1- CLINICAL USES Protectives are used for
  non-specific mouth ulceration such as aphthus
  ulcer
• It is usually combines with local anesthetic and
  antiseptics such as ORAL B composed of
• -lidocaine, cetylpyridinium, menthol cineole
• 2- examples of oral protectives
• Carmelose gelatin (ORABASE)
• Choline salicylate dental gel (BOJELA)
• Benzdamine (DIFFLAM)

102

• ANTI-SEPTIC MOUTH RINSE

1- Chlorhexidine 2- Cetylpyridinium chloride
Triclosan 3- phenols 4- Hexitidine (oraldene
mouth rinse) 5- Domiphen bromide (Bradoral
lozenges)
103

• CHLORHEXIDINE 0. 2 CORSODYL Hexidine

• 1- PROPERTIES OF CHLORHEXIDINE
• It is used in 0.2 as mouth rinse
• It is the most effective mouth rinse
• It Reduces gingival pathogen
• The anti-microbial last several hours
• it is effective in gingivitis associated with
  bleeding PUS
• it cause permanent stain of restorative
• But reversibly stains natural teeth dorsum of
  the tongue

104

• CHLORHEXIDINE 0. 2 CORSODYL Hexidine

• 2- MOA
• It broad spectrum antiseptic
• its bacterial action exerts by disruption of
  bacterial membrane of both gram positive
  negative bacteria
• 3- CLINICAL USES
• Oral hygeine especially if there heavy plaque
• Inhbition of plaque formation
• Gingival infection
• It may help in recurrent aphous ulcer

105

• CHLORHEXIDINE 0. 2 CORSODYL Hexidine

• 4- ADVERSE EFFECTS
• Reversible brown staining of natural teeth
• Irreversible brown staining of artificial teeth
  (restorative)
• Idiosyncratic Epithelial irritation of oral
  cavity
• Rarely parotid gland swelling
• Inflammation of salivary glands
• It may mask periodontitis

106

• CETYLPYRIDINIUM CHLORIDE0.5
• SCOPE

• 1-PROPERTIES
• It is surface active agent
• It is ineffective in present of bleeding, sputum
  pus
• It is weak antibacterial
• 2- MOA
• It acts as detergent which help removal of
  bacteria Disrupts the membrane of bacteria

107

• PHENOLS
• CHLORASEPTICS

• It contains phenol
• Available as spray , mouth rinse lozenges
• 2- ADVERSE EFECTS OF PHENOL
• Nephrotoxicity if exceeds the dose
• It inhibits polymerization of resin restoration
• It damage the cavity liner

108

• Agents used in dental procedures

• 1- HYDROGEN PEROXIDE
• It is used for root canal irrigation
• Its action is mediated by releasing nascent
  oxygen which kills bacteria
• 2- SODIUM HYPOCHLORITE 5
• It is used to irrigate root canal
• It is irritant to mucous membrane of oral cavity

109

• Agents used in dental procedures

• 3- OBTUNDANTS
• A- DEFINTION OF OBTUNDANT
• Chemical precipitates cellular protein of nerve
  fiber
• Causing paralysis of nerve fiber which leads to
  diminish sensation of dentine
• B- IDEAL PROPERTIES OF OBTUNDANTS
• Acts without initial pain
• Does not stain teeth, dentine or enamel
• It penetrates quickly through the dentine but not
  too deep otherwise it may lead to inflammation of
  the pulp

110

• Agents used in dental procedures

• C- MOA OF OBTUNDANT
• It precipitates cellular protein of nerve fiber
• Causing paralysis of nerve fiber which leads to
  diminish sensation of dentine
• D- CLINICAL USES
• Obtundants allow painless excavation

111

• EXAMPLES OF OBTUNDANTS

• 1- Eugenol
• It causes initial stimulation followed by
  paralysis of nerve
• 2- Zinc chloride
• It stains teeth and has poor penetration
• 3- Absolute Alcohol
• It requires the oral cavity to be dry
• 4- Cresote

112

• Agents used in dental procedures

• 4- MUMIFYING AGENT
• A- Definition of mumifying agents
• It is a chemical causes aseptic dryness and
  hardness of pulp tissues and root canal
• They have astringent and antiseptic properties
• All mumifying agents are obtundant but not all
  obtundants are mumifying agents
• B- CLINICAL USES
• They applied when pulp or content of the root
  can NOT be removed

113

• EXAMPLES OF MUMIFYING AGENTS

1- Iodinated cresol 2- beta-naphthol 1 in
alcohol 3- iodoform 4- Ammonical silver nitrate
(it stains teeth) 5- Forlmaldehyde
114

• FLOURIDE PREPARATIONS

• 1- NATURAL SOURCE OF FLOURIDE
• Water (1PPM iseffective cincentration)
• Fish (20 PPM)
• Tea (100 PPM)
• 2- METABOLISM ABSORPTION OF FLOURIDE
• Calcium and magnesium decrease flouride
  absorption
• Flouride concentrates in bone teeth
• In children, the flouride concentrates in bone
  and teeth than elderly

115

• FLOURIDE PREPARATIONS

• 3- MECHANISM OF ACTION OF FLOURIDE
• Flouride converts hydroxyapatite to FLOUROAPATITE
  which leads
• Makes the apatite structure more stable which
  improve CRYSTALLINITY of the structure
• FLOUROAPATITE is less soluble in acid
• FLOURIDE inhibits bacteria enzymes

116

• EXAMPLES FLOURIDE PREPARATIONS

• 1- ACIDULATED PHOSPHATE FLOURIDE (APF)
• It contains flouride between 10,000 to 20,000
  PPM
• It is the preparation of choice for professional
  flouride application
• It benefits last 2-3 years after application on
  the teeth
• Contact time upon application is (1-4 minutes)
  depends on the type of preparation.

117

• EXAMPLES FLOURIDE PREPARATIONS

• ACIDULATED PHOSPHATE FLOURIDE (APF)
• A- Advantages of APF
• Stable in solution
• Not irritant to gingiva
• Agent of choice for professional application
• B- Disadvantages of APF
• APF is acidic solution may affect CEMENTUM
• Not suitable for dentrifrices

118

• EXAMPLES FLOURIDE PREPARATIONS

• 2- SODIUM FLOURIDE
• It is available in tablets such as Zymaflour
  1mg
• 0.25 MG (1/4 Tablet) per day required for 5-16
  years old
• A- Advantages of sodium flouride
• Stable in solution
• Neutral solution (Ph 7.0)
• B- Disadvantages of sodium flouride
• It is NOT compatible with many abrasives in
• tooth-paste because
• - it reacts with CALCIUM PHOSPHATE
• - and becomes insoluble compound
• - Not absorb into circulation (not effective)

119

• EXAMPLES FLOURIDE PREPARATIONS

• MOUTH RINSE CONTAINS SODIUM FLOURIDE
• It is more effective than MFP present in
  tooth-paste
• but combination of sodium flouride mouth rinse
  with dentrifrices are more effective than either
  product alone
• Mouth rinse containing FLOURIDE 100 PPM
  recommend to use it twice daily
• Mouth rinse containg 250 PPM used once daily
• mouth rinse contains 1000 ppm used once weekly
  or every other week (???

120

• EXAMPLES FLOURIDE PREPARATIONS

• 3- SODIUM MONOFLOUROPHOSPHATE (MFP)
• It is commonly used in tooth-paste
• A- Advantages of (MFP)
• Stable in various pH
• It is compatible with tooth-paste abrasives
• B- Disadvantages of (MFP)
• It is weak flouride source
• Efficacy is questionable

121

• EXAMPLES FLOURIDE PREPARATIONS

• 4- STANNOUS FLOURIDE
• A- Advantages of STANNOUS FLOURIDE
• Both cation anion are effective
• B- Disadvantages of STANNOUS FLOURIDE
• Unstable in solution
• Stain teeth
• bitter taste

122

• TOXICITY OF FLOURIDE

• A- ACUTE TOXICITY
• It is common during applying APF IN CHILDREN
• Fatal dose 50-225 mg/kg
• Symptoms of toxicity
• - Nausea, vomiting
• - Abdominal pain
• - Sweating
• - Convulsion
• - Death

123

• TOXICITY OF FLOURIDE

• B- CHRONIC TOXICITY
• It is occurs at concentration ranges between 2-8
  ppm consumed in drinking water
• Flourosis occurs when the crown of permanent
  teeth are forming
• DEFINITION OF FLOUROSIS
• - Is hypoplastic defect resulting from
  disturbance in the function of AMELOBLAST
  (enamel) during teeth development
• Symptoms of chronic toxicity
• - endemic flourosis is associated with
• - mottled enamel deformed teeth

124

• DENTRIFERICES

• 1- It is a pharmaceutical preparations are used
  locally on the teeth oral cavity to perform the
  followings
• Clean
• Polish
• Prevent bacterial fermentation
• Prevent gingivitis
• Prevent dental caries

125

• EXAMPLES OF DENTRIFERICES

• TOOTH PASTE
• POWDER
• LIQUID IN FORM OF SOLUTION

126

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 1- Abrasive
• It is am inert , insoluble and finely powdered
• Examples of abrasives
• - calcium pyrophosphate
• - dicalcium phosphate
• Main action of abrasive
• - it cleans and polish
• - removes stain and plaque

127

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 2- Flavouring agents
• They have the following properties
• good odor
• mild antiseptic
• mild local anesthetic
• counter irritant
• Examples of flavouring agents
• - peppermint
• - cinnamon
• - clove oil
• - menthol

128

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 3- SWEETNER
• Examples of sweetner
• - Saccharin
• - aspartame
• - glycerin

129

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 4- HUMICTANT
• FUNCTIONS OF HUMICTANTS
• - Keep moisture of the tooth-paste
• - prevents dryness of the tooth paste
• - it gives plasticity to the tooth-paste
• - it has demulcent action on the gum
• Examples of sweetner
• GLYCERIN
• SORBITOL

130

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 5- DETERGENT FOAMING AGENTS
• FUNCTIONS OF HUMICTANTS
• - they lower surface tension(emulsifying
  agents)
• - emulsify fatty materials
• - Promote good penetration and mixing
  of constituents of the tooth-paste
• - they assists in removal mucous deposit
  and debris
• - Help to dissolve plaque

131

• TOOTH-PASTE

MAIN INGREDIENTS OF TOOTH PASTE EXAMPLES
DETERGENT FOAMING AGENTS Examples of
detergent and foaming agents - sodium
lauryl-sulfate - magnesium
lauryl-sulfo-acetate - monoglyceride
- dioctyl-sodium-sulfo-succinate
132

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 6- THICKENING AGENTS
• FUNCTIONS
• - Improve maintain the consistency of the
  paste
• - they prevent separation of the tooth-paste
  contents under extreme temperatures (high low)
• Examples of thickening agents
• - glycerin starch
• - carboxy-methyl-cellulose
• - sodium alginate
• - methyl-cellulose

133

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 7- PRESERVATIVES
• FUNCTIONS
• - prevent bacterial , fungal growth which
  prevents fermentation of the tooth-paste
• Examples of preservatives
• - methylparaben 0.15
• - propylparaben 0.15

134

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 8- FLOURIDE
• FUNCTIONS
• - It is anti-cariogenic agent and
  significantly reduces caries
• - it is commonly used sodium-mono-flouro-phosp
  hate (MFP) because
• it is stable at various Ph
• compatible with many abrasives

135

• TOOTH-PASTE

• MAIN INGREDIENTS OF TOOTH PASTE
• 9- DESENSITIZING AGENTS
• Not present in most of tooth-paste
• examples of desensitizing agents
• - Potassium nitrate
• - Potassium oxalate

136
GLUCOCORTICOIDS

• Adrenal steroids are synthesised from zona
  fasciculata of adrenal cortex as needed
• It is stimulated by ACTH which is release from
  pituitary gland
• ACTH is regulated by CRF in hypothalamus
• Glucocorticoids is synthesised from chlosterol
• Stress also stimulate glucocorticoids

137
Adrenal Gland
138
(No Transcript)
139
Glucocorticoids
140
MECHANISM OF ACTION

• Glucocorticoids bind with specific receptors in
  the cytoplasms
• The complex binds with DNA which leads to
• prevent transcription such as
• - COX-2
• - Block Vit D3 mediated induction of
  
• osteocalcin
• or induce particular gene
• - Such as LIPOCORTIN-1 Tyrosine hydroxylase

141
MECHANISM OF ACTION

• Glucocorticoids bind with specific receptors in
  the cytoplasms
• The complex binds with DNA which leads to
• prevent transcription such as
• - COX-2
• - Block Vit D3 mediated induction of
  
• osteocalcin
• or induce particular gene
• - Such as LIPOCORTIN-1 Tyrosine hydroxylase

142
Direct effects come from receptor binding
CBG
albumin
HSP70
IP
IP
HSP70
HSP90
HSP90
transcription
GRE GRE
GRE GRE
Altered cellular function
protein
143
Example of indirect inhibition of gene
induction
Cytokines
COX-2
NOS-2
NF-
B
?
NF-
?
B
TNFR
TNF-
?
NF-
?
B
I
?
B
?
GCR
GC
I
?
B
?
I
?
?
B
GCR
GLUCORTICOIDS
144
Phospholipase A2
(PAF)
145
(No Transcript)
146

• Pharmacological action of glucocorticoids
• 1- General effects on metabolism
• - Water, edlectrolyte balance and organ systems
• 2- Negative feedback on Pituitary Hypothalamus
• 3- Anti-inflammatory and immunosuppressive

147

• GENERAL METABOLIC SYSTEMIC EFFECTS
• 1- Carbohydrate and protein metabolism
• 2- Decrease glucose utilization
• 3- increase gluconeogenesis which may induce
  hyperglycemia
• 4- Decrease in protein synthesis breakdown
• 5- It has permissive effects on the lipolytic
  response to catecholamines

148

• GENERAL METABOLIC SYSTEMIC EFFECTS
• 6- Redistribute fat in large dose
• 7- It has some mineralocorticoids activities
• 8- Increase calcium secretion decrease its
  absorption
• 9- Reduce function of osteoblast
• 10- and Increase the activity of osteoclast
  (Digest bone)
• by hypocalcemia-induced parathyroid
  hormone secretion
• These lead to osteoporosis

149

• NEGATIVE FEEDBACK EFFECTS
• 1- Both endogenous and exogenous glucocorticoids
  have a negative feedback on CRF ACTH
• 2- The inhibitory effects of endogenous
  glucocorticoids due to exogenous steroids is
  prolonged (months)
• 3- lipocortin-1 play negative feedback on
  hypothalamus and pituitary
• 3- and leads to atrophy of adrenal cortex

150

• Atrophy due to negative feedback inhibition of
  ACTH

3rd
vent
( - )
( )
CRF neuron
IL-1 IL-2 IL-6 TNF-?
( - )
( )
immune system
ACTH
( )
( - )
Adrenal
d
Cortisol
administered glucocorticoid
151

152

• Anti-Inflammatory
• 1- Inhibit production of prostaglandins due to
  decrease the expression of COX-2
• 2- inhibit early and late manifestation of
  inflammation
• 3- Which leads to prevent chronic inflammation
• 4- Decrease fibroblast which leads to inhibition
  of chronic inflammation (less fibrosis) and wound
  healing and repair

153

• Continue anti-inflammatory effects
• 5- Inhbits Phospholipase A2 by inducing
  lipocortin which leads to
• Decrease production of PAF
• Arachidonic acid which is the precursor for
• Production of prostaglandins
• Leukotrienes (slow reacting substance
  of anaphylaxis

154
Continue anti-inflammatory effects 6- Decrease
histamine release 7- decrease production of
nitric oxide 8- Decrease production of PAF 9-
Decrease the production of GM-CSF which is
essential for production of -platelets -Monocyte
, neutrophil eosinophil -RBCs
155
IMMUNOSUPPRESSIVE EFFECTS

• Drug binds only to certain targets
• Supress initiation generation of immune response
• It is non-selective
• Supress cellular immunity
• and Humeral
• It induces apoptosis of lymphocyte

156
ADVERSE EFFECTS OF GLUCOCORTICOIDS

• Adverse effects occur after prolonged used
• or large dose
• 1- Supress response to infection or injury
• 2- Impair wound healing
• 3-Slight incidence of peptic ulcer
• 4- Cushingsyndrome
• 5- Osteoporosis
• 6- Hyperglycemia

157
ADVERSE EFFECTS OF GLUCOCORTICOIDS
7- Muscle wasting 8- Inhibit growth in
children 9- Euphoria Psychosis 10- decrease
blood supply to bone leading to necrosis the head
of the femur inhalation
158
ADVERSE EFFECTS OF GLUCOCORTICOIDS
11- cataract 12- glaucoma 13- increase in
intracranial pressure 14- disorder of menestrual
cycle 15- oral thrush especially when taken by
inhalation 16- Adrenal insufficiency It may
take two months or more up to 18 months
159
GUIDELINES FOR GLUCOCORTICOID THERAPY
1- It should based on the severity of
diseases 2- Dosage, frequency, duration
preparation influence the response and adverse
reactions 3- Administered locally when possible
inorder to minimize the adverse effects
efficacy 4- The pharmacological dose should be
tapered in order to avoid adrenal crisis
160
CLINICAL USES OF GLUCOCORTICOIDS

• 1- Replacement therapy (Addisondisease
• 2- Asthma
• 3-Topically in various inflammatory condition
• skin , eye, nose
• 4- Post neurosurgery head and spinal injury
• 5- Autoimmune diseases
• -Inflammatory bowel disease
• - haemolytic anemia

161
CLINICAL USES OF GLUCOCORTICOIDS
6- Anti-cancer with other cytotoxic agents 7-
Autoimmune diseases 8- Inflammatory diseases
- haemolytic anemia - organ transplant
with other immunosuppressants 9- Anti-emetic in
conjunction with other anti-emetic
162
GLUCOCORTICOIDS USES IN DENTAL PRACTICE
10- Temporary relief of sympton associated
with Oral inflammation and ulcerative lesion such
as A- Recurrent aphthus stomatitis Triamcinolone
acetonide (Kenalog orabase) B- Erosive lichen
planus -- Dexamethasone C- Major aphthae -
Kenalog orabase
163
CLASSIFICATION OF GLUCOCORTICOIDS
DURATION OF ACTION Pregnancy Risk Potency
Short (8-12hrs) - Hydrocortisone - Cortisone C D 1 0.8
Intermediate (18-36) - Methylprednisolone - Prednisolone - Prednisone - Triamcinolone C C B C 5 4 4 5

164
CLASSIFICATION OF GLUCOCORTICOIDS
Duration of action Pregnancy Risk Potency
Long acting (36-54) - Betamethasone - Dexamethasone C C 25 25-30

165
INHALER GLUCOCORTICOIDS
DRUG Pregnancy Risk Potency Compare to dexamethasone1
Fluticasone C 1200
Budesonide (Pulmicort, Rhinocort) C 980
Beclomethasone (Beconase, Beclovent) C 600
Triamcinolone 330

166
SEE YOU NEXT TIME
167
Thank you