This document discusses corticosteroids, including their production in the adrenal cortex, classification, mechanisms of action, and uses. It notes that corticosteroids are produced from cholesterol and have important roles in metabolic control and stress response regulation. They are classified based on their chemical structure and can have glucocorticoid, mineralocorticoid, or androgenic effects. Corticosteroids have a wide range of therapeutic uses due to their potent anti-inflammatory and immunosuppressive properties.

2. GUIDED BY
DR KEERTHI R
PROFESSOR
ORAL AND
MAXILLOFACIAL
SURGERY
PRESENTED BY
VISHNU V GOPAL
POST GRADUATE
STUDENT
OMFS

3.  According to the National Institute of General
Medical Sciences, the term "steroid" is a chemical
name for any substance that has a characteristic
chemical structure consisting of multiple chemical
rings of connected atoms. Some common
examples of steroids are:
►Vitamin D
►cholestrol
►estrogen
►cortisone

4.  INTRODUCTION
 HISTORY
 ANATOMY AND PHYSIOLOGY OF ADRENAL GLAD
 BIOSYNTHESIS
 CLASSIFICATION
 PHARMACOKINETICS
 PREPARATION AND DOSAGES
 INDICATIONS
 USES IN OMFS
 ADVERSE EFFECTS
 CONTRAINDICATIONS
 CONCLUSION

5.  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.
 These have glucocorticoid, mineralocorticoid, and
weakly androgenic activities.
 Conventionally the term corticosteroid, or corticoid
include both natural gluco and mineralocorticoid and
their synthetic analogues

6.  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.

7. 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

8.  An inner medulla, is a source
of catecholamine – adrenaline
and nor-adrenaline
 Chromaffin cell is the principal
cell type
 Medulla is richly innervated by
sympathetic fibres and is
considered as extension of
sympathetic nervous system
 Medulla develops from
ectoderm (neural crest)
An outer cortex, which
secretes several classes of
steroid hormones including
Glucocorticoids and
Mineralocorticoids
Three different concentric
zones of cells that differ in
major steroid hormones they
secrete
Cortex develops from
mesoderm
• The two adrenal glands are located immediately anterior to the kidneys,
encased in a connective tissue capsule and usually partially buried in an island
of fat. Their combined weight is about .01-.02% of total body weight in both
males and females.

12.  Adrenal cortex makes and secretes over 30 different steroid
hormones(collectively called corticosteroids).Corticoids are 21
carbon compounds having a cyclopentanoperhydro-
phenanthene(steroid) nucleus. Since adrenal cortical cells store
only minute quantity of hormone ,rate of release is governed by
the rate of biosynthesis.

14.  The hypothalamic-pituitary-adrenal (HPA) axis is a feedback loop
that includes the hypothalamus, the pituitary and the adrenal glands.
The main hormones that activate the HPA axis are corticotropin-
releasing factor (CRF), arginine vasopressin (AVP) and
adrenocorticotropin hormone (ACTH). The loop is completed by the
negative feedback of cortisol on the hypothalamus and pituitary
DIURINAL RHYTHM
 ACTH is secreted in irregular pulses throughout the day which cause
parallel increases in plasma cortisol . Both the frequency and the
amplitude of the pulses are the greatest in the early morning.
 This early morning increase in ACTH release is initiated by the
release of CRH (corticotropin releasing hormone) and starts
approximately a couple of hours before waking.
 The lowest levels of ACTH in blood occur just before or after falling
asleep. This results in the characteristic diurnal rhythm in ACTH and
cortisol secretion

16.  Glucocorticoids
Cortisol-5 – 30 mg
Corticosterone- 2 – 5 mg
 Mineralocorticoid
Aldosterone - 5 – 150 mcg
11- deoxycorticosterone- Trace
 Sex Hormones
Androgen – DHEA - 15 – 30 mg
Progestogen – Progesterone - 0.4 – 0.8 mg
Oestrogen – Oestradiol - Trace

17. Direct Actions
Permissive Actions
 •Lipolytic effects
 •Effect on BP
 •Effect on bronchial muscles (e . g .
sympathomimetic amine)

18.  Pharmacological Actions
1. Mineralocorticoid actions
2. Glucocorticoid actions
Carbohydrate
Protein
Lipid
calcium metabolism
CVS
Skeletal muscle
CNS
Stomach
Respiratory system
lymphoid tissue and blood cells
Inflammatory responses
Immunological and allergic responses
Growth & Cell Division

22. Lipid metabolism
Permissive action
Promote adipokinetic
agents activity(lipolysis)
Redistribution of Fat
Moon face , fish mouth ,
buffalo hump
Calcium metabolism
↓ Intestinal absorption
↑Renal excretion
OSTEOPOROSIS-spongy
bones are more
sensitive(e.g., vertebrae, ribs
etc)
Cardiovascular system
Restrict capillary permeability
Maintain tone of arterioles & Myocardial
contractility
Na+ sensitize blood vessels to the
action of catecholamines &
angiotensin-(permissive role in
development of hypertension ,should be
used cautiously in hypertensives)
CNS
Direct:
Mood(mild euphoria),Behaviour,Brain
excitability,High doses lower seizure
threshold-cautious use in epileptics
Indirect:
maintain glucose, circulation and
electrolyte balance

23.  Skeletal muscle
Optimum level of corticosteroid is
needed for
normal muscular activity.
Hypocorticisim :
↓ work capacity & weakness(due to
hypodyanamic circulation)
Hypercorticism :
•excess mineralocorticoid action -
hypokalemia – weakness
•excess glucocorticoid action - muscle
wasting & myopathy -weakness
Stomach
↑ section of gastric acid &pepsin&↓ in
PG levels in the stomach--
Cytoprotective effect of PG lost--result-
-peptic ulcer
Misoprostol ( A prostaglandin
E1, analogue) may be used to replenish
the depleted stomach PGS

24.  Lymphoid tissue and Blood cells
•Lymphoid tissue:
• ↑ rate of destruction of lymphoid cells(T cells are more sensitive than B cells)
•Blood cells:
↑ number of RBCs,platlets,neutrophils in
circulation. ↓ lymphocytes,eosinophils and basophils blood count come back
normal after 24 hours.
 Inflammatory responses
Irrespective of type of injury the attending inflammatory response is ↓ed.The
cardinal signs of inflammation –redness,heat,swelling and pain are
suppressed.
In early events:↓acute inflammatory response, reduced exudation, ↓ in
numbers and activity of leucocytes, ↓ in inflammatory mediators.
In late events:↓numbers and activity of mononuclear cells and fibroblasts, ↓
proliferation of blood vessels, less fibrosis-thus ↓ chronic inflammation but
also ↓ healing.

26. Growth & Cell division
Delays the process of healing and scar formation.
Retards the growth of children.
 Respiratory system
•Most potent and most effective anti-inflammatory
•Effects not seen immediately (delay 6 or more hrs)
•Inhaled corticosteroids are used for long term control in bronchial asthma.
 Effects on stress
 ACTH and cortisol secretion are increased by stressful stimuli including
surgery , trauma, pain, apprehension, infection, hypoglycaemia and
haemorrhage. The increase in cortisol production is necessary for
survival, and stresses that are normally tolerated can become fatal in
adrenal insufficiency Rapid deterioration resulting in organ damage and
shock/coma/death can occur, especially in children

27.  This process takes 30-60 min.So effects of corticosteroids are not
immediate ,and once the appropriate proteins are synthesized-effects
persist much longer than steroid itself

28.  Glucocorticoids
Short acting
Intermediate acting
Long acting
Mineralocorticoids
Inhalant steroids
Topical steroids
SYNTHETIC STEROIDS have largely replaced the
natural compounds in therapeutic use ,because they
are potent,longer acting,more selective,for
glucu/mineralo action and have high oral activity.

29. ►Corticosteroids are generally grouped into four classes, based on
chemical structure.
►Allergic reactions to one member of a class typically indicate an
intolerance of all members of the class.
 "Coopman classification“
 Given after S. Coopman who gave the classification in 1989
CLASSSIFICATION OF STEROIDS

30. ►Group A
Hydrocortisone, Hydrocortisone acetate, Cortisone
acetate, Tixocortol pivalate, Prednisolone,
Methylprednisolone, and Prednisone.
►Group B
Triamcinolone acetonide, , Mometasone, Amcinonide,
Budesonide, Desonide, Fluocinonide, Fluocinolone
acetonide, and Halcinonide.

31. ►Group C
Betamethasone, Betamethasone sodium phosphate,
Dexamethasone, Dexamethasone sodium phosphate, and
Fluocortolone.
►Group D
Hydrocortisone-17-butyrate, Betamethasone valerate,
Betamethasone dipropionate, Prednicarbate and
Fluprednidene acetate

32.  Routes of adm: of Corticosteroids
►1. Topical steroid for use topically on the skin,
eye, and mucous membranes.
►2. Inhaled steroids for use to treat the nasal
mucosa, sinuses, bronchi, and lungs.
►3. Oral forms - such as prednisone and
prednisolone.
►4. Systemic forms - available in injectable for
use intravenously and parenteral routes

33. Potency Examples
Highest 0.05% Clobetasol propionate
0.05%Betamethasone dipropionate
High 0.1% Halcinonide
0.25% Desoximethasone
0.05% Fluocinonide
0.5% Triamcinolone acetinode
0.05% Betamethasone
dipropionate
0.05% Diflorasone diacetate cream
Intermediate 0.2% Fluo-cinolone acetonide
0.05% Desoxymethasone
0.025% Betamethasone benzoate
0.2% Hydrocortisone valerate
Low 0.025% Fluo-metholone
0.025% Triamcinolone acetonide
0.03% Fluocinolone pivalate
0.01% Betamethasone valerate
Lowest 0.25-2.5% Hydrocortisone
0.5% Prednisolone

34. Agent Antiinflammatory Topical
Equivalent
oral dose
(mg)
Forms
Available
Hydrocortisone 1 1 20 O,I,T
Cortisone 0.8 0 25 O
Prednisolone 5 4 5 O,I
Triamcinolone 5 5 4 O,I,T
Flu-
prednisolone
15 7 1.5 O
Betamethasone 25-40 10 .6 O,I,T
Dexamethasone 30 10 .75 O,I,T

35. Injectable:
Betamethasone Dexamethasone
Prednisolone Methylprednisolone
Hydrocortisone Triamcinolone
Oral:
Betamethasone Fludricortisone
Prednisolone Prednisone
Methylprednisolone
Topical:
Betamethasone Clobetasol
Flucinolone Mometasone
Inhalation:
Beclomethasone Budesonide
Flunisolode

36. Triamcinolone
Kenacort,
Tricort,
kenalog,
Tess buccalpaste
Oral:1,4,8mg syrup
Topical:0.1% eye
drops,ointment
Parentral: 3,10,40
mg/ml for I.M,
intraarticular,
Intralesional
injections

37. Dexamethasone
 Decadron,
 Dexasone,
 Wymesone
Oral:0.25,0.5,0.75,1,2,4,6mg tablets
Topical:0.1% eye drops, ear drops,
skin ointment
Parenteral: 4,8,10,20 mg/ml for IV,
IM, intralesional and intraarticular

38.  Betamethasone
 Betnesol,
 Betnovate,
 Betnesol forte,
 Betawin forte,
 Walacort,
 Stemin
Oral: oral drops – 0.5 mg/
ml, tablets – 0.5 to 1 mg.
Topical – 0.1% eye drops,
ointment,0.05% nasal drops,
0.12% skin creams
Parenteral:4 mg/ml for IM,
IV, intralesional,
intraarticular

39. Hydrocortisone
 Wycort,
 Hycort,
 Unicort,
 Cipcorlin,
 Efcorlin
Oral:5mg,10mg,20mgta
b
Topical:
1%eye drops
0.025%nasal drops
0.25-2.5%skin cream
Parenteral:25, 50 mg/ml
for
IV,IM,SC Injections

40.  Cortisone
 Corlin,
 Cortone
Oral: 5, 10, 25
mg
tablets
Parentral:22,25
mg/ml of
solution

41.  Prednisolone
 Wysolone,
 Prelone,
 Nucort,
 Cecort,
Oral:5,10, 20 mg tablets,
15mg/5 ml syrup, 5mg/ml
suspension as pediatric
drops
Parenteral:25,50 mg/ml
IM,IV,Intralesional

43. Acute 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.
Chronic adrenal insufficiency
• 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

44. • 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 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 doses can be high in
severe illness

45. Arthritis
Rheumatoid arthritis
Osteoarthritis
Rheumatic fever
Gout
Collagen diseases
SLE
Polyarteritis nodosa
Dermatomyositis
Nephrotic syndrome
Glomerulonephritis
Severe allergic reactions
Used for short periods in
anaphylaxis
Angioneurotic edema
Utricaria
Serum sickness
Autoimmune disorders
Autoimmune hemolytic anemia
Thrombocytopenia
Active chronic hepatitis
Myasthenia gravis

46. Bronchial asthma
Status asthmaticus
Severe chronic asthma
Infective diseases
Severe forms of tuberculosis
Severe lepra reaction
Certain form of bacterial
meningitis
Pneumocystitis carini
pneumonia with
hypoxia in AIDS patients
Eye diseases
Effective in diseases of
anterior chamber
Allergic conjuctivitis
Iritis
Keratitis
Skin diseases
Eczematous skin diseases
Pemphigus vulgaris
Exfoliative dermatitis
Steven johnsons syndrome

47. Intestinal diseases
Ulcerative colitis
Chron’s disease
Others
Cerebral edema
Malignancies
Organ transplantation
and skin allograft
Shock
To test the adrenal
pituitary axis

49.  Steroids are used in :
 Impactions
 Extractions
To control post operative pain and swelling
 In maxillofacial trauma
 In malignancies and other disorders

50.  Prevention of postoperative pain, edema,
trismus after 3rd molar surgery.
 Prevention of postoperative edema after
orthognathic, and reconstructive surgery after
trauma.
 Prevention of alveolar osteitis.
 Other than this steroids are used in many other
conditions which are encountered as an oral
and maxillofacial surgeon.

51.  Abducent nerve palsy from trauma or edema
systemic steroids are used for treatment.
 Orbital apex syndrome is treated by
corticosteroids and decompression.
 Steroids are also used in treatment of
traumatic superior orbital fissure syndrome.
 Used In traumatic facial nerve palsy in
temporal bone fractures.
 Steroids eye drops are used to reduce swelling
and pain in eye after transconjuctival approach
For orbital floor repair etc.
Steroids in maxillofacial trauma

52.  Ulcerative,Vesiculoerosive diseases
 Erosive lichenplannus , RAS
 Benign lesions
• Eg: CGCG
 Salivary gland disorders
• Eg: Mucocele
 TMJ Disorders
• Eg: Osteoarthritis
• Rheumatiid arthritis
 Neuralgia Treatment
• Eg. Post herpatic neuralgia
 Miscellanous
• OSMF
Steroids used in other conditions

53. 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 clinical features are ulceration and reddening, with pain that can
be severe and debilitating.
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).

54.  Short course of Topical Corticosteroids accelerate remission
without adverse effects in conditions like :
Recurrent aphthous stomatitis (RAS), some cases of erythema
multiforme (EM), and Drug-induced ulceration.
 Topical Corticosteroids must be used for longer, less predictable
periods in conditions like :
Severe RAS, Erosive oral lichen planus (OLP), specific forms of EM,
and mucous membrane pemphigoid (MMP)
 In very severe cases of ulcerations the treatment can be started by
short courses of systemic corticosteroids followed by
maintainance regimen of topical steroids or can be started
simultaneously.

55.  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.

56. Factors that influence the effectiveness of Topical Corticosteroids:
 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
which is explained in article by (Regezi and Sciubba, 1999).
 The contact time between the drug and lesion and the vehicle used
to apply it.
 Concentration which can increase its clinical effectiveness,
although no additional advantage is obtained beyond certain
limits.
 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.

57.  Systemic steroids for ulcerative
vesiculobullous diseases:
 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.
 Pemphigus Vulgaris
• Mainstay 1-2mg/kg/day Initial dose of treatment – 0.5 mg/kg/day
to 3 mg/kg/day Dose that achieves clinical control is maintained for
2-3 weeks and then gradually tapered.
 Erythema multiforme : minor : treted by steroid 20-40mg /day for
4-6 days
major: 60mg/day slowly tapered to 10/mg
day for 6 weeks

58.  Cicatrical phemphigoid
Prednisolone 20-60mg/day to stop new bullae formation , then
tapered by 20% every 2-3 week until it resches dose of 10mg and the
dose is maintained on alternate days and reduced by 5mg every 2
weeks and the stopped .
 Bullous pemphigoid
Clobetasol propionate 20 -40 mg/day is more effective for the
treatment.
 Lichen planus
Prednisolone 1mg/kg/d for <7 Days Tapered to 10-20mg per day for
2 weeks.
 Lupus erythematosus
Predisolone – 20 - 30 mg/day for 2- 6 weeks Tapered gradually.

59.  CGCG
Intralesional injection of triamcinolone can be given in a
dose of 1 to 2 mg/kg/day (maximum of 60 mg). The
treatment interval at 4 to 6 weeks.
 Hemangioma
Prednisone at a dose of 20-30 mg/d can be given for 2
weeksto 4 months ( Fost and Esterly)Intralesional
triamcinolone acetonide (4 mg/mL) (Hawkins et al)

60.  Mucocele
0.05% clobetasol propionate 3 times a day for 4
weeks in a mucosal adhesive base. Intralesional
injections have also been tried with success.

61.  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)

62.  Rheumatoid arthritis
Intraarticular injection – 10 to 40 mg/ml
 Osteoarthritis
Intraarticular injection – 20 mg/ml(2 injections 14
days apart)

63.  Bell’s palsy
Significant improvement can be achieved 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.
 OSMF
Prednisolone – 20 - 30 mg/day for 2 – 4 weeks Gradually taper
Discontinue in 1- 2 months
Injections of triamcinolone 10mg/ml diluted in 1 ml of 2% lidocaine with
hyaluronidase 1500 IU, biweekly for 4 weeks. (Borle et al)
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.

64. Mineralocorticoids:
Sodium and water retention
Edema
Hypokalemic alkalosis
Progressive rise in B.P
Weight gain
Fluid and electrolyte disturbance
Glucocorticoid:
 GIT:
Acute erosive gastritis with hemorrhage
Peptic ulcer
Intestitial perfortion
Pancreatitis
 Metabolic effects:
Hyperglycemia
Ketoacidosis
Hyperosmolar coma
Hypophosphatemia

65.  CVS and renal system:
Hypertension
Salt and water retention
Hypokalemic alkalosis
 CNS:
Influence mood, sleep pattern
Insomnia
Acute psychotic reactions
Benign intracranial hypertension
Epilepsy
 Musculoskeletal effects:
Proximal myopathy and osteoporosis with compression
fractures of vertebrae
Acute aseptic necrosis of bone
 Eyes:
Glaucoma

66.  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.
 Relative Contraindications:
Peptic ulcer
Diabetes mellitus
Hypertension
Pregnancy
Herpes simplex
Tuberculosis
Osteoporosis
Psycosis
Epilepsy
Renal failure

67.  Rule of 2
Adrenocortical suppression should be
suspected if a patient has received
Glucocorticoid 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

68.  Barely three years later after the discovery of steroids ,
Fraser and co-workers reported the death of a34-year-old
man after routine orthopaedic surgery due to shock, adrenal
insufficiency, and circulatory collapse. The patient had been
on corticosteroids for rheumatoid arthritis, but the treatment
had been stopped prior to surgery.
 Surgery-activation of HPA axis
Surgery is one of the most potent stressors that can cause
activation of the HPA axis. The degree of activation depends on
the type and duration of surgery and anesthesia, with many
other variables, including analgesics, antihypertensive
medications, infections, and age. The maximum stimulation of
the HPA axis is occur during reversal of anesthesia and in the
immediate postoperative period.

69.  Significant hypotension
Significant hypotension which cannot be explained
by acute blood loss, myocardial infarction, anesthesia, drugs, or
electrolyte imbalance should suggest the possibility of an acute
adrenal insufficiency. This is especially true if the blood
pressure does not respond promptly to blood transfusions or
vasopressors.
It is suggested that an increase in capillary resistance and
potentiation of the effect of vasoconstrictors on blood vessels
may be factors in the blood pressure response to adrenal
corticosteroids

70. Lack of increase in cortisol production during stress
would cause the host to succumb to it. On the other hand,
too much cortisol would be detrimental, causing increased
tissue breakdown, poor wound healing, and
immunosuppression.
Given this background, it is clear that any patient who
has inadequate cortisol production in response to surgical
stress will fare poorly in such a situation. This patient will
need to be recognized, and his acute steroid requirement
will have to be estimated and supplemented

71.  Preoperative considerations
 Adrenocortical function may be suppressed if: The patient
is currently on daily systemic corticosteroids at doses above
7.5 mg prednisolone(or equivalent).
Cortisteroids has been taken regularly during the past 30
days.
Corticosteroids have been taken for more than one month
during past one year.
Although the evidence for the need of steroid cover may be
questionable, medico legal and other considerations suggest
that one should act on the side of caution and fully inform and
discuss with patient, take medical advice in case of doubt, give
a steroid cover unless confident that collapse is unlikely.

72.  B.P. must be carefully watched during surgery and
especially during recovery and steroid
supplementation must be given if B.P. starts to fall.
 Drugs especially sedative and GA ,are a hazard and
it is extremely important to avoid hypoxia,
hypotension and haemorrhage
 Patient may also require special management as a
result of diabetes, hypertension ,poor wound healing
and infections.

73. Procedure No steroids for
previous 12
months
Steroids taken
during previous 12
months
Steroids currently
taken
Conservative
dentistry or
dentoalveolar
surgery ↓LA
No cover required Give usual oral
steroids dose in
morning or
hydrocortisone 25-
50mg I.V. preop
Double oral steroids
dose in morning or
hydrocortisone 25-
50 mg I.V
preop, continue
normal steroid
medication postop
Intermediate
surgery(multiple
extractions,or
surgery ↓GA)
Consider cover if
large doses of
steroids were given
Give usual steroids
dose in morning
+hydrocortisone 25-
50 mg i,.v. preop +
i.m. 6 hourly for 24 h
Double oral steroid
dose in morning
+hydrocortisone 25-
50mg I.Vpreop +
i.m.6 hourly for
24h,then continue
normal med.
Maxillofacial surgery
or trauma
Consider cover if
large doses were
given
Same+i,.m 6 houly
for 72 h
Same +I. M 6 hourly
for 72 h+normal
thereafter

74.  Conducting treatment in the morning.
 Control of anxiety and emotional stress.
 Use long-acting anaesthetics.
 Treatment of postoperative pain.
 Minimum use of NSAIDs
 Asepsis surgery ,Antibiotic prophylaxis
 Prevention of iatrogenic fracture during
surgery .
 Topical steroids for use in mouth predispose to
oral candidiosis.

76.  Hyperactivity can cause:
Cushings syndrome
Hyperaldosteronism
Adreno genital syndrome

77.  Due to hyper secretion of glucocorticoids
particularly cortisol.
 Due to pituitary origin its cushings disease.
 Due to adrenal origin its cushings syndrome.

78.  Disproportionate body fat
distribution
 Moon face
 Buffalo hump
 Pot belly
 Purple striae
 Thinning of skin
 Pigmentation
 Facial redness
 Hirsutism
 Muscle weakness
 Bone resorption
 Hyperglycemia
 Hypertension
 Susceptiblity to infections
 Poor wound healing

79.  Can be due to adrenal cause (primary)
 Can be due to extra adrenal cause ( secondary)
 Increase in ECF volume and blood volume
 Hypertension
 Severe depletion of potassium
 Muscle weakness
 Metabolic alkalosis

80.  Addison's disease
 Adrenal crisis
 Chronic adrenal hyperplasia
 Addison’s disease
Failure of adrenal cortex to secrete all the
corticosteroids
Primary : due to adrenal cause
Secondary : failure of anterior pituitary to secrete
ACTH.
Tertiary: failure of hypothalamus to secrete CRF.

81.  Pigmentation of skin
and mucous membrane
 Muscle weakness
 Dehydration
 Hypotension
 Decreased cardiac
output
 Hypoglycemia
 Nausea, vomiting,
diarrhoea
 Inability to withstand
stress
Addison's disease

82.  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
Causes
Exposure to even mild stress Hypoglycaemia due
to fasting surgical operation Sudden withdrawal
of glucocorticoid treatment

83.  Congenital adrenal hyperplasia
Congenital disorder characterized by increase in
size of adrenal cortex.
Even though the size of the gland increases the
cortisol secretion decreases.
Congenital enzymes necessary for synthesis of
cortisol, particularly 21- hydroxylase. cortisol, particularly 21-
hydroxylase.
 In boys:
Precocious body growth, causing stocky
appearance called infant Hercules
Precocious sexual development with enlarged
penis even at age of 4 years.
 In girls:
Produces Masculinization
Female child born with external genitalia of male
type.

84. • 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.