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Chapter 6: Inflammation & Anti-inflammatory Drugs R, :red_cross:…
Chapter 6:
Inflammation & Anti-inflammatory Drugs
INFLAMMATION
Inflammation is the body’s response to injury or infection.
AIM
1) Destroy harmful invaders
2) Remove irritants
3) Prepare tissue for healing
Five Signs of Inflammation
PAIN
Dolor
HEAT
Calor
REDNESS
Rubor
SWELLING
Tumor
LOSS OF FUNCTION**
Functio Lessa
MECHANISM OF INFLAMMATION
CELL INVOLVED
1) Macrophage
2) Neutrophils
3) Eosinophils
4) Lymphocytes
CHEMICAL MEDIATORS
1)
Histamine
and
serotonin
(vasoactive amines)
2)
Bradykinin
(peptide)
3)
Eicosanoids
(e.g.,
prostaglandins, thromboxanes, leukotrienes
).
EICOSANOIDS FORMATION
When there is
inflammatory stimulus or hormones
MEMBRANE PHOSPHOLIPID BILAYER
Released
ARACHIDONIC ACIDS (AA)
LEUKOTRIENES
PROSTAGLANDIN
TROMBOXANE
PROSTAGLANDIN
1 more item...
by
5-lipoxygenase
pathway
by
cyclooxygenase
CYCLO-OXYGENASE (COX)
3 more items...
by Phospholipase A2
action
ANTI-INFLAMMATORY
DRUGS
Non-steroidal anti-inflammatory drugs
(NSAIDs)
Inhibit
synthesis of Prostaglandin, leading to
decreased pain, swelling, and inflammation.
Anti-inflammatory, analgesic, antipyretic and antiplatelet
(aspirin) properties
Treatment of
pain
(headache, toothache, myalgia, backpain),
fever, arthritises and dysmenorrhoea
Contraindicated to
pregnancy, peptic ulcers, viral infections mainly in children, hypersensitivity reactions and hemophilic patients.
NON-SELECTIVE COX INHIBITOR
Acetylsalicylic acid (aspirin)
Indomethacin
Naproxen
Mefenamic acid
Diclofenac sodium
Piroxicam
PREFERENTIAL COX-2 INHIBITOR
Nimesulide
Meloxicam
Nabumetone
Some activity against COX-1
SELECTIVE COX-2 INHIBITORS
Celecoxib
Parecoxib
Pofecoxib
Cause little
gastric mucosa damage
.
Do not inhibit platelet aggregation.
Highly selective inhibitors
of COX-2 enzyme.
Potent
anti-inflammatory action
Have
analgesic & antipyretic
properties
Lower
incidence of gastric upset
Steroidal anti-inflammatory drugs (SAIDs)
SECRETED FROM ADRENAL CORTEX
controlled by
Renin Angiotensin
Aldosterone System
MINERALOCORTICOIDS
Cortisol, Hyrocortisone
(Zona Fasciculata)
Effect:
Na, K, H and water
homeostasis to control
electrolyte and water balance.
stimulate the
reabsorption of Na+ & secretion of K+&H+
No major role
in managing inflammation and allergy
No role
in repair injury, managing stress and manage pain
controlled by
ACTH
GLUCOCORTICOIDS
Aldosterone
(Zona Glomerulosa)
Effect:
Metabolism of
carbohydrates,
fats and proteins
stimulate
gluconeogenesis
anti-inflammatory & anti-allergic
effect
useful to
repair injury and manage stress
assist to
reduce pain
AS ANTI-INFLAMMATORY DRUGS
Injectables, Oral, Topical and Inhalation Preparation
Suppress T Lymphocyte
Prevent mast cells, basophils, and eosinophils from releasing various chemical mediators
of inflammation, including
histamine, prostaglandins, leukotrienes
, and other substances that cause tissue damage, vasodilation, and edema.
Stabilize, lysosomal membranes
and
prevent the release of catabolic enzymes
from these organelles.
Cause
vasoconstriction and decrease capillary permeability
by direct actions as well as
inhibiting the actions of kinins, bacterial toxins, and chemical mediators
released from mast cells and eosinophils.
Suppress lymphoid tissue
and
reduce the number of circulating lymphocytes
(eosinophils, basophils, and monocytes)
Increasing the concentration of
erythrocytes, platelets, and polymorphonuclear leukocytes.
:warning:
ADVERSE EFFECTS OF
CORTICOSTEROID AGENTS
:warning:
Fluid and Electrolyte Disturbance
– sodium and water retention
Precipitation of Diabetes mellitus
– hyperglycaemia
Increased susceptibility to infections
– immune response suppression
Peptic ulceration
– bleeding & perforation
Osteoporosis
– flat spongy bones
Myopathy
– weakness of muscles
Glaucoma
– prolonged topical therapy
:no_entry:
CORTICOSTEROID
WITHDRAWAL
:no_entry:
SYMPTOMS
Headache
Dizziness
Fainting
Fatigue
Lethargy
Joint Pain
Nausea
Weight loss
Faver
Hypoglycemia
Infection
Hypothalamic-pituitary-adrenal (HPA)
axis is
SUPPRESSED
due to
exogenous steroid
use.
This is because
Cortisol and Glucocorticoids inhibit CRH & ACTH release.
When we stop exogenous steroid, the adrenal gland did not release sufficient steroid hormones called as
ADRENAL SUPRESSION/ INSUFFICIENCY
due to the supression of HPA
ADRENAL SUPRESSION/ INSUFFICIENCY
is caused by
rapid tapering/cessation/stop
of
exogenous steroid.
In some
AUTOIMMUNE DISEASE
, it may cause
FLARE
of symptoms :fire:
TO FIX :Gradual withdrawal or tapering
of the dose is to allow recovery of the
normal pituitary-adrenal responsiveness
to the secretion of endogenous corticosteroid
WITHOUT
exacerbating the underlying disease state.
:red_cross:
NSAIDs
:red_cross:
ADRENAL SUPRESSION/ INSUFFICIENCY
TO DETECT:
hormone stimulation test
TO PREVENT:
minimizing corticosteroid dose and duration
