2. 2
Contents
Introduction
History
Functional anatomy and histology of adrenal
glands
Biosynthesis of steroids
Fate of steroids
Mineralocorticoids (source, action, regulation)
Glucocorticoids (source, action, regulation)
Mechanism of action at cellular level
3. 3
Classification of steroids
Uses in medicine
Steroids in dentistry
Adverse effects
Drug interactions
Precautions
Pathologies of adrenal gland
4. 4
Introduction
The adrenal gland is the source of a diverse group
of hormones essential for metabolic control,
regulation of water and electrolyte balance, and
regulation of body’s response to stress.
Using cholesterol as a substrate, the adrenal cortex
produces a large number of substances collectively
known as corticosteroids.
5. 5
History
By the middle of 19th century it was demonstrated
that adrenal glands were essential for life
Later, it was appreciated that the cortex was more
important than the medulla
A number of steroidal active principles were
isolated and their structures were elucidated by
kendall and his coworkers in the 1930s.
6. 6
However, the gate to their great
therapeutic
potential
was
opened by Hench (1949) who
obtained striking improvement
in rheumatoid arthritis by
using cortisone.
The nobel prize was awarded
the very next year to kendall
and Hench.
Currently, corticosteroids are
drugs with one of the broadest
spectrum of clinical utility.
10. 10
Zones of adrenal
cortex
Zona glomerulosa
Hormones
Aldosterone
Desoxycorticosterone
Zona fasciculata
Cortisone
Cortisol
Zona reticularis
Dehydroepiandrosterone
Androstenidione
Traces of estrogens
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
13. 13
Rate of secretion of the principal
steroids
Glucorticoids
10-20 mg daily
Mineralocorticoids –
0.125 mg daily
Textbook of Medical Physiology 11th Edition,
Arthur C. Guyton, John E. Hall - 2006
14. 14
REGULATION OF SECRETION
Regulation by Hypothalamus
(CRH) & Pituitary (ACTH)
Negative feedback effect
from plasma cortisol levels
Pulsatile secretion of ACTH
based on Circadian rhythm
Neural effects on HPA axis
due to emotional / physical
stress
15. 15
Fate of corticosteroids
Degraded mainly in liver
Conjugated to form glucuronides and to a lesser
extent form sulphates
25% - excreted in bile and feces
75% - excreted in urine
16. 16
MECHANISM OF ACTION
plasma memb CYTOPLASMIC
Corticosteroids
RECEPTOR
PROTEIN
GLUCOCORTICOID
RESPONSE
ELEMENT
Transcription of
m - RNA
New protein
synthesis
Nucleus
TOTAL
TIME
30 – 60 mins
18. 18
Mineralocorticoids
Source : Zona glomerulosa
Functions: 90% of mineralocorticoid activity is
provided by aldosterone
Aldosterone – life saving hormone
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
19. 19
Actions
On Na+ metabolism
• Increase in the
reabsorption of sodium
from renal tubules
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
20. 20
On ECF volume
• Na reabsorption from renal tubules
• Simultaneous water reabsorption
• Increase in ECF volume
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
21. 21
On BP
• Increases ECF volume
• Increases BP
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
22. 22
On K+ ions
•Increase in the
excretion of
potassium from renal
tubules
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
23. 23
On H+ ion concentration
• Causes tubular secretion
of hydrogen ions
• Essential to maintain
acid - base balance
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
25. 25
Regulation of aldosterone secretion
Increase in K+ concentration
Decrease in Na+ Concentration
Decrease in ECF volume
Decrease in K+ concentration
Increase in Na+ Concentration
Increase in ECF volume
Feedback
inhibition
Stimulation
angiotensinogen
Angiotensin - 1
Angiotensin - 2
Renin
Converting
enzyme
Juxtaglomerular
apparatus
Excretion of K+
Retention of Na+
Retention of water
Lungs
kidneys
Adrenal cortex
Aldosterone
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
27. 27
Glucocorticoids
Source : zona fasciculata
Functions:
Hormone
Glucocorticoid activity
Cortisol
95%
Corticosterone
4%
Cortisone
1%
Cortisol – Life protecting hormone
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
28. 28
Actions:
On carbohydrate metabolism
• Increases blood glucose
level in two ways,
Promotes gluconeogenesis
Inhibits glucose uptake
and utilization by
peripheral cells
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
29. 29
On protein metabolism
• Promote catabolism of
protein in cell
• Increase plasma amino
acid and protein
content in the cell.
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
30. 30
On fat metabolism
• Causes mobilization and redistribution of
fat
• Actions are
• - Mobilization of fatty acids from adipose
tissue
• - Increase the concentration of fatty acids
in blood
• - Increases the utilization of fat for energy
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
31. 31
On mineral metabolism
• Enhances sodium retention
• Slightly increase potassium
excretion
• Decreases blood calcium by
inhibiting absorption from
intestine
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
32. 32
On water metabolism
• Accelerate the excretion
of water
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
33. 33
On muscles
• Increase the release of
aminoacids from
muscles by catabolism
of proteins
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
34. 34
On blood vessels
• Decreases the number of
circulating eosinophills in
retculoendothelial cells
• Decrease the number of
basophils and lymphocytes
• Increase the number of
neutrophills, RBCs and platelets.
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
35. 35
On vascular response
• Glucocorticoids is essential
for the constrictor action of
adrenaline and noradrenaline
• In adrenal deficiency, the
blood vessels fail to respond
to Adr and NA leading to
vascular collapse.
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
36. 36
On CNS
• Essential for normal
functioning
• Insufficiency causes
personality changes like
irritablity and lack of
concentration
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
37. 37
Permissive action of
glucocorticoids
• The action of some hormones are
executed only in the presence of
glucocorticoids.
• Eg: Calorigenic effect of glucagon
• Lipolytic effect of catecholamines
• Pressor effects of catecholamines
• Bronchodialation by catecholamines
Essentials Of Medical Physiology 3rd Edition,
K Sembulingam
38. Anti-inflammatory actions
Lipocortin
Recruitment of WBC & monocytemacrophage into affected area &
elaboration of chemotactic
substances
ELAM & ICAM in endothelial cells
TNF from phagocytic cells
IL1 from monocyte-macrophage
Expression of cyclooxygenase II
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
38
40. On resistance to stress
Physical or mental stress
Increases ACTH
Increase in glucocorticoid
secretion
High resistance to body
against stress
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
40
41. 41
Anti allergic action
• Suppress all types of hypersensitivity and
allergic phenomena.
• Suppression of recruitment of leucocytes at
the site of contact with antigen and of
inflammatory response to immunological
injury.
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
42. 42
Immunosuppresive
effects
• Suppress the immune system of the
body by decreasing the number of
circulating T lymphocytes.
• Prevent release of interleukin-2 by T
cells
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
45. 45
Mechanism of action at cellular
level
Translocation of glucose transporters
from plasma membrane to deeper sites
Decreased glucose
uptake and
utilization in
peripheral tissues
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
46. 46
Induction of hepatic
gluconeogenetic enzymes
Increased
production of
glucose from
aminoacids
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
47. 47
Induction of hepatic glycogen
synthetase
Deposition of
glycogen in
hepatocytes
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
48. 48
Site specific changes in sensitivity
of adipocytes to GH, Adr, insulin
Altered
distribution of
body fat
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
49. 49
Decreased expression of POMC
gene in pituitary corticotropes
Decreased
production of
ACTH
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
50. 50
Induction of lipocortins in macrophages,
endothelium and fibroblasts
Lipocortins inhibit
phospolipase A2 –
decreased production
of PGs,LTs&PAF
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
51. 51
Negative regulation of genes for cytokines in
macrophages, endothelial cells and
lymphocytes
Decreased production of IL1,2,3,6,TNFα,GM-CSF,
Interferon – γFibroblast
proliferation and T lymphocyte
function are suppressed.
chemotaxis interfered.
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
52. 52
Decreased production of acute phase reactants
from macrophages and endothelial cells
Complement
function is
interfered.
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
53. 53
Decreased production of ELAM-1
and ICAM-1 in endothelial cells
Adhesion and
localization of
leukocytes is
interfered.
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
54. 54
Inhibit IgE mediated histamine
and LT-C4 release from basophils
Effects of antigen –
antibody reaction
not mediated
GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF
THERAPEUTICS - 11th Ed. (2006)
69. 69
Replacement therapy:
Acute adrenal
insufficiency
Chronic adrenal
insufficiency :
• Hydrocortisone
or
dexamethasone
are given i.v, first
as a bolus
injection and
then as infusion
along with istonic
saline and
glucose solutions.
• Hydrocortisone
given orally is the
most commonly
used drug with
adequate salt and
water allowance
Congenital adrenal
hypoplasia :
• 0.6 mg/kg daily
in divided doses
round the clock
70. 70
Pharmacotherapy:
• Single dose (even excessive) is not harmful can be
used to tide over mortal crisis even when benefit is
not certain.
• Short courses (even high doses) are not likely to be
harmful in the absence of contraindications.
Starting doses can be high in severe illness
71. 71
• Long term use is potentially hazardous: keep the
dose to minimum which is found by trial and error,
even partial relief may have to be tolerated.
• No abrupt withdrawal after a corticoid has been
given for > 2 to 3 weeks: may precipitate adrenal
insufficiency
77. 77
Infective diseases
Severe forms of tuberculosis
Severe lepra reaction
Certain form of bacterial meningitis
Pneumocystitis carini pneumonia with
hypoxia in AIDS patients.
83. 83
Steroids in oral surgery
Prevention of postoperative pain,
edema, trismus after 3rd molar
surgery
Prevention of postoperative
edema after orthognathic surgery
Prevention of alveolar osteitis
84. 84
steroids in Endodontics
Steroids are used as intracanal medicaments in
endodontics
Ledermix is corticosteroid- antibiotic intracanal
paste
Painful teeth with acute apical periodontitis that
had been dressed with ledermix paste gave rise to
less pain and it has proved to be an effective
intracanal medicament for the control of
postoperative pain associated with acute apical
periodontitis with a rapid onset of pain reduction
International Endodontic Journal,Volume 36
Issue12, Pages 868 - 75
87. 87
Ulcerative Vesiculoerosive diseases
Immunologically mediated diseases that affect the oral
mucosa present with inflammation and loss of
epithelial integrity, through cellular and/or humoral
immunity-mediated attack on epithelial connective
tissue targets.
The
main
reddening,
debilitating.
clinical
with
features
pain
that
are
can
ulceration
and
be
and
severe
88. 88
• Corticosteroids play a central role in the treatment
of vesiculoerosive lesions.
• However, the frequency and severity of the adverse
effects associated with the use of systemic
corticosteroids have led to the increased use of
topical corticosteroids (TCs)
89. 89
Criteria for use
short course of
TCs
Accelerate
remission without
adverse effects
TCs must be used
for longer, less
predictable periods
Recurrent aphthous
stomatitis (RAS), some
cases of erythema
multiforme (EM), and
Drug-induced
ulceration.
Severe RAS, Erosive
oral lichen planus
(OLP), specific forms of
EM, and mucous
membrane pemphigoid
(MMP)
Scully et al., 1999; Chan et al., 2002
90. 90
CODS Davangere
24/01/2014
very severe cases
of ulceration
Short course of systemic
corticosteroids followed
by maintenance regimen
of TCs and or can also be
started simultaneously
with the systemic
therapy
Pemphigus
vulgaris ,10-30%
of Pemphigoid
patients, Erosive
lichen planus
Inevitably be treated with
systemic corticosteroids
and/or other
immunosuppressant
therapies
Laskaris and Angelopoulos, 1981;
Nisengard and Neiders, 1981; Fine et al., 1984;
Domloge-Hultsch et al., 1994; Dayan et al., 1999
91. 91
Protocols for use
When a TC is prescribed, and especially when a prolonged
course is predicted, the basic rule is that a TC of a potency
appropriate to the severity of the clinical symptoms should
be used, at the lowest possible concentration and frequency,
with maintaining the effectiveness of the treatment.
It should always be taken into account that these drugs do
not cure the disease but rather control or relieve the
symptoms.
JDR April 2005 vol. 84 no. 4 294-301
92. 92
The key factors
The specific diagnosis
The severity of the oral disease
The presence or absence of extra-oral lesions
The medical history of the patient
JDR April 2005 vol. 84 no. 4 294-301
93. 93
Factors that influence the effectiveness
of TCs:
The intrinsic potency of the drug
which can be significantly increased
by the halogenation of the steroid;
esterification, which makes the drug
more lipophilic and gives it greater
penetrability
(Regezi and Sciubba, 1999).
JDR April 2005 vol. 84 no. 4 294-301
94. 94
Factors that influence the
effectiveness of TCs:
The contact time
between the drug and
lesion and the vehicle
used to apply it;
JDR April 2005 vol. 84 no. 4 294-301
95. 95
Factors that influence the effectiveness
of TCs:
Concentration
which can increase its clinical
effectiveness, although no
additional advantage is
obtained beyond certain limits.
(Regezi and Sciubba,
1999).
JDR April 2005 vol. 84 no. 4 294-301
96. 96
Success of a topical medicine
Two main factors
Number of applications per
day
High-potency
(2-3 times)
The vehicle
used
Low potency
(5-10 times)
JDR April 2005 vol. 84 no. 4 294-301
Various
vehicles
97. 97
Various vehicles.
Orabase (Stoy, 1966),
Cyanoacrylate (Jasmin et al., 1993),
Bioadhesive patches made of cellulose
derivatives (Mahdi et al., 1996),
Gels (Regezi and Sciubba, 1999), and
Denture adhesive paste (Lo Muzio et al., 2001).
JDR April 2005 vol. 84 no. 4 294-301
98. 98
Patients prescribed TC in an adherent vehicle
should be instructed to
Apply a small amount to the target area after
meals, and
Not to eat or drink for at least 30 min.
It is best not to rub the TC in, because this can
produce irritation.
JDR April 2005 vol. 84 no. 4 294-301
99. 100
• For small and accessible erosive lesions, or those
located on the gingiva and palate, the lesions can
be treated by the
• Use of an adherent paste in a tray,
• Which allows for accurate control over the contact
time and
• Ensures that the entire lesional surface is exposed
to the drug.
JDR April 2005 vol. 84 no. 4 294-301
101. 102
major aphthae or severe multiple
minor aphthae
• Prednisone therapy should be started at 1.0
mg/kg/day
in patients with severe RAU and should be
tapered after
1 to 2 weeks.
Natah SS, Konttinen YT. IJOMS 2004;33:221-34.
102. 103
Erythema multiforme
Minor EM
Severe or rapidly
progressing
lesions
20 – 40 mg/day for 4 – 6
days
60 mg/day slowly
tapered by 10 mg/day
over 6 weeks
Indian J Ophthalmol Jan-Feb 2010;58(1):64-66
103. 104
Pemphigus Vulgaris
• Mainstay 1-2mg/kg/d.
• Initial dose of treatment – 0.5 mg/kg/day to 3 mg/kg/d
• Dose that achieves clinical control is maintained for 2-3 weeks
and then gradually tapered.
Burkit’s Oral Medicine, 11th edition
104. 105
Pulse therapy
• Also called short term therapy
• High dose therapy involves a 48-72 hrs course of
intensive steroid administration
• Single i.v injection of a supra-physiological dose of
steroid
• Dose of 0.5-2g of prednisolone or
equivalent
105. 106
Benefits
• Avoids complications & side effects of long term steroid
therapy
• To achieve immunosuppressive effects similar to those
with higher doses of steroids
106. 108
Cicatricial pemphigoid
Predisolone – 30
to 60 mg/day
2-3 weeks to stop
new bullae
formation
Tapered by 20%
every 2-3 weeks
until the dose of
10 mg is reached
Dose maintained on
alternate days and
reduced by 5 mg
every 2 weeks, then
stopped
111. 113
CGCG
Intralesional injection of triamcinolone
can be given in a dose of 1 to 2 mg/kg/d
(maximum of 60 mg).
The treatment interval at 4 to 6 weeks.
J Med Assoc Thai 2008; 91 (Suppl 3): S90-6
112. 116
Hemangioma
Prednisone at a dose of 20-30
mg/d can be given for 2 weeks
to 4 months
( Fost and Esterly)
Intralesional triamcinolone
acetonide (4 mg/mL)
(Hawkins et al)
116. 122
Post herpetic neuralgia
To reduce incidence of post herpetic neuralgia:
Prednisolone 20 to 30 mg/day for 7 – 10 days
tapered to 10 mg/day for 1 week
(Treatment of oral diseases, George Lascaris)
120. 128
Bell’s palsy
Significant improvement can be
achived when Prednisolone is started
within 72 hours of symptom onset
1 mg/kg body weight (maximum 70
mg) in divided doses with meals for
six days, and the dose can be reduced
gradually over the next four days.
122. 130
Injections of triamcinolone 10mg/ml
diluted in 1 ml of 2% lidocaine with
hyaluronidase 1500 IU, biweekly for 4 weeks.
(Borle et al)
123. 131
Biweekly submucosal injections of a combination of
dexamethasone
(4mg/ml)
and
two
parts
of
hyaluronidase, diluted in 1.0 ml of 2% xylocaine by
means of a 27 gauge needle, not more than 0.2ml
solution per site, for a period of 20 weeks.
Significant relief of burning sensation (88%) and
improvement of trismus (83%) can be seen in most
patients.
124. 132
Adverse effects
Due to extention of pharmacological action occuring with prolonged
therapy
Mineralocorticoids:
Sodium and water retention
Edema
Hypokalemic alkalosis
Progressive rise in B.P
Weight gain
Fluid and electrolyte disturbance
129. 137
Suppression of inflammation and immune response:
Latent infection may flare
Oppurtunistic infection with low grade pathogens
Retardation of linear growth:
Occurs in children who receive more than 50 mg
of cortisone per m2 of body surface per day.
134. 142
During therapy:
Prescribe drug with food
Diet low in calories and sodium and rich in potassium
Check periodically for weight gain, hypertension,
hyperglycemia
135. 143
Increase dose in case of stress
Instruct patient not to stop abruptly
While stopping therapy:
Taper therapy
136. 144
Rule of 2
Adrenocortical suppression should be
suspected if a patient has received
Glucocoticoid therapy through two of the
following methods
In a dose of 20 mg or more of cortisone or
its equivalent
Via oral or parenteral route or a
continuous period of 2 weeks or longer
Within 6 months -2 years of therapy
Medical emergencies in dental office, Stanley F.Malamed
Complications in Anesthesia - John L. Atlee; Page-132
138. 146
Dental
Procedure
Previous
Systemic
Steroid Use
Routine
procedures
If prior usage
No
lasted for > 2
supplementatio
weeks and ceased n needed
< 14–30 days
ago, give
previous
maintenance
dose
If prior usage
ceased > 14–30
days
ago, no
supplementation
needed
Current
Systemic
Steroid Use
Daily
alternating
Systemic
Steroid Use
Current
topical
Systemic
Steroid Use
Treat on
No
steroid dosage supplementatio
day; no further n needed
supplementatio
n needed
139. 147
Dental
Procedure
Previous
Systemic
Steroid Use
Current
Systemic
Steroid Use
Extractions,
surgery, or
extensive
procedures
If prior usage
Double daily
lasted > 2 weeks dose on day of
and ceased <
procedure
14–30 days ago,
give previous
maintenance
dose
Treat on
steroid dosage
day, and give
double daily
dose on day of
procedure
If prior usage
ceased > 14–30
days ago, no
supplementatio
n needed
Give normal
daily dose on
first
postoperative
day when pain
is anticipated
Double daily
dose on first
postoperative
day when pain
is anticipated
Daily
alternating
Systemic
Steroid Use
Current
topical
Systemic
Steroid Use
No
supplementatio
n needed
140. 148
Scenario One
Patient requiring extractions
took a 7 day course of 20 mg.
of prednisone for exacerbation
of asthma one week ago
No supplementation
required. Even though the
dose was supraphysiologic,
the course of time it was
taken was less than 2 weeks
Clinical update by Naval Postgraduate Dental School, Maryland
Vol. 23, No. 7 July 2001
141. 149
Scenario Two
Patient requiring extractions is taking
10 mg of prednisone for the past year to
treat rheumatoid arthritis
This patient’s HPA axis is probably
suppressed due to supraphysiologic
dose of corticosteroids for longer
than 2 weeks. Supplement with at
least 100 mg of cortisol equivalent
(25 mg prednisone) in the morning
on the day of the surgery
Clinical update by Naval Postgraduate Dental School, Maryland
Vol. 23, No. 7 July 2001
142. Scenario
Three
Patient requiring extractions is
taking 2.5 mg of prednisone daily
for the past 3 months to treat his
psoriasis
No supplementation
required. Even though the
patient has been on
prednisone for over 2 weeks,
the dose is subphysiologic
and will not adversely impact
his stress response
Clinical update by Naval Postgraduate Dental School, Maryland
Vol. 23, No. 7 July 2001
150
143. Scenario
Four
Patient requiring extractions
was previously taking 50 mg of
prednisone for Crohn’s
disease. He was on a 6-month
course of prednisone but took
his last dose 5 weeks ago
No supplementation
needed. A functional stress
response returns in 14-30
days after the last dose of
steroids
151
144. 152
Scenario Five
Patient requiring extractions
is taking 75 mg of prednisone
daily for the past 8 weeks to
treat pemphigus
No supplementation
needed as 75 mg of
prednisone is the
maximum dose equivalent
to 300 mg of endogenous
cortisol
Clinical update by Naval Postgraduate Dental School, Maryland
Vol. 23, No. 7 July 2001
149. 157
Disproportionate body fat distribution
Moon face
Buffalo hump
Pot belly
Purple striae
Thinning of skin
Pigmentation
Facial redness
Hirsutism
Muscle weakness
154. 164
Addison’s disease
Failure of adrenal cortex to secrete all the
corticosteroids
Primary
Adrenal cause
Secondary
Failure of anterior
pituitary to secrete ACTH
Tertiary
Failure of hypothalamus
to secrete CRF
155. 165
Pigmentation of skin and mucous membrane
Muscle weakness
Dehydration
Hypotension
Decreased cardiac output
Hypoglycemia
Nausea, vomiting, diarrhoea
Inability to withstand stress
156. 166
Adrenal crisis
Common symptom of addison’s disease characterized by
sudden collapse associated with an increase in need for
large quantities of glucocorticoids.
Fatal if not treated in time
157. 167
Adrenal crisis
Causes
• Exposure to even mild stress
Hypoglycemia due to fasting
Surgical operation
Sudden withdrawal of glucocorticoid treatment
158. 168
Congenital adrenal hyperplasia
Congenital disorder characterized by increase in
size of adrenal cortex.
Eventhough the size of the gland increases the
cortisol secretion decreases.
Congenital enzymes necessary for synthesis of
cortisol, particularly 21- hydroxylase.
160. 170
Conclusion
• Corticosteroids play an important role in control of pain &
inflammation associated with numerous disease states of
oral cavity.
• Currently corticosteroids are drugs with one of the broadest
spectrum of clinical utility.
• But it should never be used as a substitute to other
treatments.
• Lets keep it mind that these drugs do not cure the disease but
rather control or relieve the symptoms.
• It should be used cautiously as it is two edged sword.
Notas do Editor
The normal concentration of aldosterone in bloodis about 6 nanograms (6 billionths of a gram) per100 ml, and the average secretory rate is approximately150 μg/day (0.15 mg/day).The concentration of cortisol in the blood averages12 μg/100 ml, and the secretory rate averages 15 to20 mg/day.
Mol Cell Endocrinol. 1993 Jul;94(1):111-9.
pro-opiomelanocortin (POMC
Bronchial asthma:Status asthmaticus – give i. v, withdraw after emergency is overSevere chronic asthma – as a supplement to bronchodialators or low dose oral therapy is given for longer periodsOther lung diseases:Aspiration pneumoniaPulmonary edemaAccelerate lung maturation in foetus. Therapy may be undertaken if premature delivery is contemplated.
Cerebral edema:Due to tumours, tuberculous meningitis etc responds to corticoidsDexa or betamethasone are preferred.Malignancies:Essential component of combined chemotherapy of - Acute lymphatic leukemia - Hodgkin’s lymphoma and other lymphomasOrgan transplantation and skin allograft:High dose of corticosteroids with other immunosupressants are given to prevent rejection reaction followed by low maintenance doses.Shock:I.V glucocorticoids given in septicaemic shock To test the adrenal pituitary axis
The applications in the field of oral surgery would include,Prevention of postoperative pain, edema, trismus after 3rd molar surgeryPrevention of postoperative edema after orthognathic surgeryPrevention of alveolar osteitis
the key factors that determine the selection of a topical or systemic treatment
It also depends upon the concentration
Logically, the success of a topical medicine depends mainly on the contact time of the drug with the lesion.
TCs have been applied in various vehicles. 2.1 Lotion 2.2 Shake lotion 2.3 Cream 2.4 Ointment 2.5 Gel 2.6 Foam 2.7 Transdermal patch 2.8 Powder 2.9 Solid 2.10 Sponge 2.11 Tape 2.12 Vapor 2.13 Paste 2.14 Tincture
Doses of each pulse are notstandardized but are usually 500 to 1000 mg methylprednisoloneor 100 to 200 mg dexamethasone.
Doses of each pulse are notstandardized but are usually 500 to 1000 mg methylprednisoloneor 100 to 200 mg dexamethasone.
Doses of each pulse are notstandardized but are usually 500 to 1000 mg methylprednisoloneor 100 to 200 mg dexamethasone.
1 mg /kg/day for 7 daysFollowed by reduction of 10mg each subsequent dayBurkits 11th edition
Normal HPA suppression recovery may take time to 30 days to 12 month But according to the guideline given by John L. Atlee it is considered normal to return in 6 months