Download IN THE NAME OF GOD Systemic Effects of Oral Glucocorticoids

IN THE NAME OF GOD
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Side effects from glucocorticoids are mostly
seen with oral and injectable glucocorticoids,
but can be seen with inhaled and topical
steroids at higher doses.
glucocorticoid toxicity is related to both the
average dose and cumulative duration of use.
Toxicity of Glucocorticoids
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Mild hirsutism
Bruising
Facial erythema
Increased sweating
Thin, fragile skin
Impaired wound healing
Striae
Acne
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moon face
buffalo hump
central obesity
Truncal and peripheral adipocytes vary in
sensitivity to the glucocorticoid facilitated
lipolytic effect—that is, the peripheral
adipocytes are more sensitive to this effect
than the central adipocytes.
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Cataract
Glaucoma
Exophthalmos
Swelling of lids and ocular muscle
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Ischemic heart disease
Heart failure
Atherosclerosis
Hypertension
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The pathogenesis is multifactorial,involving
increased peripheral vascular sensitivity to
adrenergic agonists, increased hepatic
production of angiotensinogen (renin
substrate), and activation of renal
mineralocorticoid receptors.
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Glucocorticoids increase hepatic glucose
production (in part by increasing substrate
availability through proteolysis and lipolysis);
they also induce insulin resistance and
hyperinsulinemia and inhibit glucose
transport into the cells.
New-onset diabetes occurs in patients with
underlying impaired glucose tolerance or
subclinical diabetes.
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Serum lipids, both triglycerides and
cholesterol, may be increased during
corticosteroid therapy.
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Peptic ulcer disease
Candidiasis
Pancreatitis
Fatty liver
Viseral perforation
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There was no increased incidence of PUD in
those taking corticosteroids alone but there
was an increased risk in those taking nonsteroidal anti-inflammatory drugs .
when a patient is prescribed corticosteroid
treatment who has risk factors for PUD such
as a past history of PUD; smoking; high
alcohol intake; or receiving ulcerogenic
drugs(NSAIDS ) should be given a
prophylactic agent for GI bleeding .
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Polycythemia is a feature of Cushing’s
syndrome but does not appear to be a feature
of corticosteroid therapy.
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The total white blood count is increased in
patients on corticosteroids. The various
classes of white blood cells are affected in the
following ways:
Polymorphonuclear leucocytes increased
Lymphocytes decreased; T cells are reduced
to a greater extent than B cells although
immunoglobulin synthesis is also decreased
Monocytes decreased
Eosinophils decreased
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Steroids act in multiple ways to inhibit the
immune system and so their use is associated
with an increased susceptibility to infection.
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Corticosteroid use is associated with sodium
and water retention; this can be reduced by
recommending a low salt diet.
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The greatest rate of bone loss occurs in the
first 6 months and is thought to continue at a
lower rate for as long as steroids are used.
Bone loss is greatest in trabecular
(cancellous) bone, which is more
metabolically active but also occurs in cortical
bone.
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Reduced osteoblast activity resulting in
reduced bone formation
Increased bone resorption due to increased
osteoclast activity
Reduced intestinal absorption of calcium and
phosphate
Reduced renal reabsorption of calcium
Secondary hyperparathyroidism
Reduced sex hormones
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A substantial increase in fracture risk can
occur within 3-6 months of steroid
treatment. If steroids are discontinued, bone
improves substantially after 6-24 months. It
seems that bone loss is related to the dose of
glucocorticoids.
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During corticosteroid use there is a reduction
in muscle protein synthesis and protein
catabolism; therefore, muscle weakness and
loss of bulk can occur. In its extreme form a
steroid myopathy may develop, affecting the
proximal muscles in upper and lower
extremities .
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Osteonecrosis (avascular necrosis) is a
serious complication of corticosteroid .The
risk increases with both dose and duration of
treatment but it is not possible to predict who
will be affected.
The femoral head is most frequently involved
but other large joints may be affected. Joint
pain and stiffness are the earliest symptoms.
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Mood swings
Euphoria
Depression
Delirium
Memory impairment
Suicide attempts
Sleep disturbance, insomnia and unpleasant
dreams
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Psychosis has been reported and usually
develops within 2 weeks of starting
treatment, particularly with doses of >40
mg/day prednisolone. Symptoms respond to
tapering of the corticosteroids, usually within
3 weeks.
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Exogenous glucocorticoids can lead to HPA
suppression and secondary adrenal
insufficiency (isolated glucocorticoid
deficiency with normal aldosterone secretion).
The abrupt cessation, or too rapid
withdrawal, may cause symptoms of AI.
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Any patient with Cushingoid appearance
Any one who has received more than 20 mg
prednisone daily (or equivalent) for more than
3 weeks
Any one who has received an evening dose of
prednisone (even physiologic) for more than
3 weeks
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No need for testing, and these patients
should be treated like any patient with
secondary AI by giving stress dose of
glucocorticoids perioperatively.
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Any patient who has received any dose of
glucocorticoids for less than 3 weeks
Any patient on less than 5 mg prednisone,
provided that it is not taken in the evening
Alternate glucocorticoid therapy
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We try to limit the adverse effects of
glucocorticoids by the following steps:
Use of the lowest dose of glucocorticoids for the
shortest period of time needed to achieve the
treatment goals
Treatment of those pre-existing comorbid
conditions that may increase risk when
glucocorticoids are required
Monitoring of patients under treatment for
adverse effects that may benefit from additional
intervention
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Pre-existing conditions or risk factors for
adverse effects that should be assessed or
treated when glucocorticoids are to be
instituted include :
Diabetes mellitus
Hyperlipidemia
Hypertension
Heart failure
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Glaucoma and Cataract
Low bone density or Osteoporosis
Peptic ulcer disease
Use of non-steroidal anti-inflammatory drugs
Presence of infection
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During treatment with glucocorticoids and
depending upon individual risk factors such as
dose and duration of glucocorticoids usage
,other medications being used ,and
comorbidities,particular attention should be
given to
Body weight
Blood pressure
Heart failure and peripheral edema
Serum lipid
Diabetes or glucose intolerance
Glaucoma
Fracture risk
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