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Culture Documents
All Pharma Summary
All Pharma Summary
ACE inhibitors
EXAMPLES
Ramipril,
Lisinopril
USES
Hypertension
Heart Failure
Post MI
Beta-Blockers
Calcium
Channel
Blockers
Atenolol,
Propanolol
Hypertension
Angina
Arrhythmias
Stable heart failure
Dihydropines
Amlodipine,
Phenyalkylamin
es Verapamil,
Benzthiazepine
sDiltiazem
Bendrofluazide,
hydrochlorothiazi
de
Hypertension
Angina
Supraventricular
arrhythmia
(Phenylalkylamines
only)
Vasodilation
block cellular entry of Ca+ by
preventing opening of
voltage-gated L-type and Ttype calcium channels
Hypertension
Combined with loop
for Heart Failure
Loop Diuretics
Frusemide,
Bumetanide
Potassiumsparing
diuretics
Spironolactone,
Amiloride
Hypertension (but
less effective than
thiazides used
when renal
impairment or
resistant to multiple
drug Tx)
Heart Failure
Secondary
Hypertension
Severe heart Failure
Thiazide
Diuretics
MECHANISM
Block ATIATII by binding to
the site on the enzyme that
normally accommodates the
terminal leucine of ATI.
Inhibits vasoconstriction.
SIDE EFFECTS
Hypotension
Dry cough
(increased
bradykinin)
Renal failure in pts
with bilateral renal
stenosis
block -adrenergic receptors inhibiting
Provocation of
the
asthma, heart
effects of adrenaline and nonadrenaline.
failure.
1 (heart) blockage decreases HR Cold hands
and
Bradycardia contractility, 2 (bronchial and
fatigue
vascular
smooth muscle) blockage causes
vasodilation.
Flushing, headache,
P.oedema
Phenyalkylamines
can worsen heart
failure
Gynaecomastia
Impotence
Hypokalaemia
Hyponatraemia
Hypotension
Gout
Type II DM
Hypokalaemia
Hyponatraemia
Hypotension
Gout
Hypokalaemia
Hyponatraemia
Abdominal
discomfort
Angiotensin II
receptor
antagonists
Losarten,
Valsarten
Alphaadrenorecepto
r antagonists
Doxazosin,
Prazosin
Hypertension
Alternative to ACE
inhibitor in heart
failure
Hypertension (in
addition to other
hypertensives)
Vasodilation by inhibition
at the angiotensin II receptor
Usually mild
No cough like in
ACE inhibitors
Reduces peripheral
resistance by inhibiting 1adrenoreceptor-mediated
vasoconstriction.
Postural
Hypotension
Dizziness
Fibrinolytics
Thrombolysis
Acute MI, stroke, PE
Nausea/vomiting
Bleeding
Antiplatelet agents
Asprin
Prevention and
treatment of MI and
stroke.
Haemorrhage
Clopidogrel
Prevention and
treatment of MI and
stroke.
Haemorrhage
Anticoagulants
Warfarin
Prophylaxis+treatme
nt DVT, PE
Prophylaxis of
embolization in AF,
Rheumatic disease +
prosthetic valves.
Haemorrhage
Heparin
Treatment of DVT,
PE. Prophylaxis of
DVT/PE post op.
MI.
Prevention of
cardiovascular
disease
Haemorrhage
Myopathy (muscle
ache)
Disturbed LFTs
Abdominal pain
Statins
Nitrates
Potassium
channel
activators
Streptokinase
Atorvastatin,
Simvastatin,
Pravastatin
Glyceral trinitrate
(GTN), Isosorbide
mononitrate
Nicorandil (only
licensed one)
Prophylaxis and
Treatment of angina.
LVF
Prophylaxis of
angina
Postural
hypotension
Tachycardia
Headache
Flushing
Dizziness
Headache
Quinidine,
Disopyramide,
Procainamide
VT
WPW
Lignocaine,
Mexiletine,
Phenytoin
Ventricular arrythmi,
especially VT
Class Ic
Flecainide
Pre-excitation AF
cardioversion of
paroxsms,AVNRT
,AVRT, WPW, AF ,
AT , NSVT (nonsustained VT)
Class II
Beta blockers
(see above also)
Junctional
tachyarrhythmias,
Paroxysmal
events,AF, Flutter,
NSVT, SVTs.
rate of spontaneous
depolarisation of SA and AV
nodal tissue
conduction through AV
node
Class Ib
GI disturbances
Hypotension
Nausea and
Vomiting
CNS toxicity
Hypotension
Bradycardia
CNS toxicity
Hypotension
Proarrythmogenic
after recent MI
may increase
mortality
Provocation of
asthma, heart
failure.
Cold hands
Class III
Amiodarone,
Bretylium, Sotalol
(Beta blocker with
class III
properties)
Amiodarone : GI
disturbances.
Corneal
microdeposits,
throtoxicosis,
photosensitivity
Class IV
Calcium channel
blockers (see
above also)
AVRT, AVNRT,
Paroxysms
Flushing, headache
P.oedema
Phenyalkylamines
can worsen heart
failure
Gynaecomastia
Impotence
Intracellular Ca2+
overload
junctional escape
beats, junctional
Digoxin
AF
Atrial Flutter
automaticity of the SA
node which slows sinus rate
refractory period of the AVN
which AV conduction
Adenosine
Atropine
Supraventricular
arrythmias
Sinus bradycardia
AV block
Cardiopulmonary
resuscitation
tachycardia,
ventricular ectopic
beats, VT.
Increased vagal
activity can cause
AT with 2:1 AVN
block
GI disturbances
Neurological
disturbances
Gynaecomastia
Bradycardia and AV
block
Malaise, flushing,
headache chest
pain, bronchospasm
Rhythm
disturbances
Constipation
Reduced Bronchial
secretions
Endocrinology-Diabetes
Insulin: Is a polypeptide containing 51 amino acids arranged in two chains (A and B) linked by Disulphide bridges. A precursor
called proinsulin, is hyrdolysed inside storage granules to form insulin and a residual C-peptide. The granules store insulin as
crystals containing zinc and insulin.
Insulin Release: Glucose is the most potent stimulus for insulin with surges at meal times. The B cells possess K+ channels
that are regulated by intra cellular adenosine triphosphate (ATP) (Katp channels). When the blood glucose increases, more
glucose enters the B-cells and its metabolism results in an increase in intracellular ATP, which closes the Katp channels. The
resulting depolorization of the B-cell initiates an influx of Ca2+ ions through you voltage sensitive Ca+ channels and this
triggers insulin release.
Insulin is destroyed the GI tract so must be given subcutaneously and IV or IM in some circumstances. Injections should be
rotated within the same region to avoid lipid hypertrophy. Absorption is fastest from the abdomen and slower from the thigh.
Insulin Regimes
1) Short acting insulin mixed with intermediate acting insulin injected subcutaneous twice daily, before breakfast and
before the evening meal/
2) Injection of intermediate acting insulin to provide background level of insulin and soluble insulin three times a day.
Short Acting Insulin
Soluble Insulin Actrapid
Simple solution of insulin
IV for
(onset 30 mins, peak
hyperglycaemic
activities 2-4hrs, subsides by
emergencies.
8hrs)
Subcutaneous
If IV effects only last 30
injection
minutes.
Insulin lispro
Humalog and
Insulin analogues have a
Blood glucose
Hypoglycaemia
and Insulin
Novorapid
faster onset and shorter
control
aspart (Rapid
Acting)
(amorphous
insulin zinc)
Lente
Humulin L or
Monotard
Isophane
Insulin (NPH)
Insulatard
Biphasic fixed
mixtures
Human mixed
(short- and
intermediateacting) insulins:
These include
Humulin 20/80,
Humulin 30/70,
Humulin 50/50,
Mixtard 20/80,
Mixtard 30/70,
and Mixtard
50/50.
Human mixed
insulin analogues
(with ultra-
Insulin auto
antibodies
Lipohypertrophy
Blood glucose
control
Suspension of amorphous
insulin zinc.
Hypoglycaemia
Hypoglycaemia
Hypoglycaemia
Hypglycaemia
short and
intermediateacting
properties):
These include
Humalog Mix25
(insulin lispro)
and NovoMix 30
(insulin aspart).
Ultralente
Humulin UL
Ultratard
Insulin
glargine
Lantus
A suspension of poorly
soluble insulin zinc crystals
that has a duration of up to
35 hours. The long duration
of ultra lente can lead to
insulin accumulation and
dangerous hypoglycaemia.
Onset of action (2-4 hrs)
Peak (6-23 hours)
Is soluble at acid pH. It has a
long peakless activity (11-12
hrs) and is given once a day.
Hypoglycaemia
Hyoglycaemia
Glitazones
Glipizide (short
half life)
Glicazide (short
half life)
Glibenclamide
(longer duration
of action)
Tolbutamide.
Rosiglitazone and
Pioglitazone
Type II diabetes
(people with ideal
weight)
Type II diabetes
given alone or in
combination with
metofrmin or
sulphonyreas in
patients who cannot
tolerate metformin
or sulphonyreas
combinations.
GI disturbance
Rashes
Hypoglycaemia
Hypoglycaemic
coma
Contraindicated in
severe
hyperglycaemia,
surgery and major
illness
Weight gain
Fluid retention
Contraindicated in
pregnancy
Acarbose
Type II diabetes
Bruising
IV bolus of 20% glucose.
Synthetic
Aldosterone
Fludrocortisone
Addisons
Hypertension
Oedema
Peptic ulcers
Mood changes
GI upset
Glaucoma
Ketoconazole
Recombinant
PTH analogue
Ergocalciferol Vit
D2
Cholecalciferol Vit
D3
Alfacalcidol
1hydroxyvitamin D
Calcitriol 1,25
Dihydroxy D
Teriparatide
Cushings
Anti fungal
Hypocalcaemia
Vit D deficiency
Hepatic necrosis
Adrenal suppression
Nausea vomiting,
abdominal
cramping pain.
Dizzyness,
drowsyness nausea
and vomiting.
Hypernaetremia
GI upset, Erosion of
Oesophagus
Hypercalcaemia
Stomach pain
Diarrhoea
Hypercalcaemia
Dehydroxyvit D at kidney.
Phaeochromocytoma Neoplasm of the adrenal medulla. 10% are malignant, 10% are extra-adrenal, 10%
are familial. Blockage of adreno receptors must be started first.
aPhenoxybenzami
An irreversible antagonist is
Tumours of adrenal
adrenorecepto ne
used to block the a-effects of
medulla
r antagonist
Labetalol
the large amounts of
catecholamines from
Doxazosin
Phentolamine
tumours of the adrenal
Prazosin
medulla.
Tamsulosin
Terazosin
Hypocalcaemia
Hypoparathyriodism
Dizzyness
Leg Cramps
Nausea
are bilateral, 10%
Reflex tachycardia
b-blockers
Atenolol (see
above)
Conns excess production of aldesterone
Aldosterone
Spironolactone
Conns
receptor
(see above)
Liver disease with
blockers
Eplernone
ascites
Postassium
Sparing
Diuretic
Zero Order
Kinetics
Amiloride
Triamterene
Potassium sparing
diuretic
Conns
Severe
Hyperkaleamia
Painful
Gyanocamastia
Severe
Hyperkalaemia
Common drugs
Phenytoin,
Aspirin, Ethanol,
Theophylline,
Thiopentone
Anti-Epileptics Epilepsy is a chronic disease in which seizures result from abnormal discharge of cerebral neurones. Epilepsy
is defined as a tendency to recurrent seizures i.e. two or more seizures. Partial seizures (seizures begin focally) Simple
(consciousness not impaired) Complex (with impairment of consciousness) Beginning as a simple partial seizure and
progressing to a complex partial seizure. Impairment of consciousness at onset. Partial seizure becoming secondary
generalised. Generalised Seizures Absence Seizure Typical (petit mal) Atypical. Others Myoclonic seizure, Clonic seizure,
Tonic seizure, Tonic-clonic seizure (grand mal) Atonic seizure.
Treatment should be considered when two or more unprovoked seizures have occurred within a short period. Whenever
possible, treatment should involve only one drug.
Generalised
Lamatrogine
Lamatrogine and
Lamatrogine
Epilepsy
Sodium Valproate
Valpraote have similar
Blurred vision
mech of action as
dizziness and
Phenytoins discussed
drowsyness. Serious
below. Valproate also
skin reactions can
seems to in increase
occur especially in
GABAergi central inhibition
children.
mechanisms that may
Valproate - Nausea,
involve stimulation of
weight gain,
glutamic acid decarboxylase
bleeding tendencies
activity and/ or inhibition of
and transient hair
GABA-T activity.
loss). The main
disadvantage is that
occasional
idiosyncractic
reactions cause
sever or fatal
hepatic failiure.
Focal Epilepsy
Carbamazepine
Phenytoin
Phenytoins anticonvulsant
action is probably a result of
its ability to prevent high
frequency repetitive activity.
Phenytoin binds prerentially
to inactivated (closed) Na+
channels stabilizing them in
the inactivated state and
preventing them from
returning to the resting
closed state which they must
do before they can open
again. High freuquency
repetitive depolarisation
increases the proportion of
Na+ channels in the
inactivated state and,
because these are
susceptible to blockade by
phenytoin, the Na+ is
progressively reduced until it
is eventually insufficient to
evoke and action potential.
Neruonal transmission at
normal frequencies is
relatively unaffected by
phenytoin because a smaller
portion of the Na+ channels
are in the inactivated state.
Carbamazepine, lamotrigine,
valproate, and topiramate.
Have similar actions on
neuronal Na+ channels.
Carbamazepine is
metabolised in the
liver to
carbamzepine10,11- epoxide, an
active metabolite
that partly
contributes to both
its anti-convulsant
action and
neurotoxicity. In
contrast to
phenytion there is a
linear increase in
serum
concentration with
dosage. Mild
neurotoxic effects
are common
(nausea dizziness
drowsyness, blurred
vision and ataxia)
Agranulocytosis is a
rarer idyiosyncratic
reaction.
Phenytoin is
hyroxylated in the
liver by a saturable
enzyme system.
The rate of
metabolism varies
greatly in patients.
And up to 20 days
maybe required for
the serum level to
stabilize after
changing the dose.
Dose is increased
gradually until fits
are prevented , or
until signs of
cerebellar
disturbance occur
(nystagmus, ataxia,
involuntary
movements) One
the metabolizing
enxymes are
saturated , a small
Absence
Epilepsy in
Children
Ethosuximide
Sodium Valproate
increase in dose
may produce toxic
side blood levels of
the drug. Other
effects Gum
hypertrophy, acne,
greasy skin,
coarsening of the
facial features and
hirsutism.
EthosuximideNausea vomiting.
Dopamine
Receptor
Agonists
Pre Synaptic
Re-Uptake
inhibitor
Bromocriptine
(ergot derivative)
Ropinirole (non
ergot derivative)
Apomorphine
(very powerful
given by
parenteral
administration)
Amantadine
Parkinsons
Prolactinomas
Parkinsons
or dance like
movement) are an
important adverse
effect.
Long term after five
years treatment
about 50% of
patients will have
lost ground. In some
there is a gradual
recurrence of
parkinsionian
akinesia. A second
form of
deterioration is the
shortening of
duration of action of
each dose. Various
dyskinesias may
appear and, with
time rapid
oscillations in
mobility and
dyskinesias.
Nausea, psychiatric
symptoms, postural
hypotension.
Pulmonary fibrosis
and retroperitoneal
fibrosis.
Apomorphine
(highly emetogenic)
domperidone should
be given before
treatment started.
Dizzyness, Loss of
co-ordindation,
inability to sleep,
nausea,
soon develops
nervousness
Inhibits monoamine oxidase
Nausea
type B (MAO-B) there by
Heartburn
increasing dopamine. This is
Dry mouth
done by reducing the
metabolism of the dopamine
in the brain potentiating the
levdopa which can be
reduced by up to one 1/3. It
is used to reduce end of dose
akinesia.
COMT
Entacapone
Inhibbits catechol-O Parkinsons
Drowsyness
inhibitors
Benzarazide
methltransferase (COMT) and
Dizzyness
prevents peripheral
Stomach upset
conversion of Levodopa to
Diarrhoea
(inactive) 3-O-methyldopa. It
increases the plasma half life
of levodopa and increases its
action.
Antimuscarini
Benzetropine
Produce a modest
Parkinsons
Dry mouth
cs
Procyclidine
iimprovement in the early
Urinary retention
Orphenadrine
stages of parkisons disease,
and constipation.
Benzhexol
but the akinesia responsible
Effect memory and
for most of the functional
concentration.
disability responds least well.
Myaesthenia Gravis An acquired organ specific autoimmune disorder in which antibodies are directed at the post synaptic
acetycholine receptor. This results in weakness and fatiguability of skeletal muscle groups. The most commonly effected
muscles are the proximal limbs and the ocular an bulbar muscles.
Oral
Prydostigmine
Most widely used drug; it has
Myaesthenia gravis
Overdose causes a
acetycholinest
a duration of about 3-5
cholinergic crisis
erase
hours. Patients response will
with severe
determine the dose required.
weakness. Colic and
Great symptomatic drug but
diarrhoea may
does not alter the natural
occur.
history of the disease.
Motor neurone disease
Riluzole
Rilutek
Used to treat amyoptrophic
MND
Nausea
lateral sclerosis. Delays the
Fatigue
onset of ventilator
Hepatitis
dependence or tracheostomy
by 2 months.
Guillain- Barres syndrome (post-infective polyneuropathy) Inflammtory demyelinating polyradiculoneuropathy. Often follows
one to two weeks after infection or diarrhoea, which may have been mild. Campylobacter jejuni has been particularly implicated
as a cause of the diarrhoea and is associated with the most severe form. Classic presentation distal paraesthesie, often with
little sensory loss, and weakness can occure proximally, distally spreading or generalised. The symptoms ascend up lower limbs
and body over days to weeks. Facial weakness present in 50% cases. In sevre cases respiratory and bulbar involvement occurs.
IF VC drops to 1 litre of below: artificial ventilation is needed.
High dose
(IVIg)
Either high-dose intravenous
Guillen Barres
Hepatitis
Monamine
oxidase
inhibitor type
B (MAO-B)
Selegiline
Parkinsons
immunoglobul
ins
immunoglobulins (IVIg) at
Renal failure
400mg/kg for 5 days or
plasmapheresis can be
administered, as they are
equally effective and a
combination of the two is not
significantly better than
either alone. Therapy is no
longer effective after 2
weeks after the first motor
symptoms appear, so
treatment should be
instituted as soon as
possible. IVIg is usually used
first because of its ease of
administration and safety
profile, with a total of five
daily infusions for a total
dose of 2 g/kg body weight
(.4kg each day).
Glaucomas- Mixed group of disorders that have some common features: Optic disc cupping, visual field loss and usually, raised
intraocular pressure (IOP).
Beta-Blockers
Timolol, carteolol,
Reduce aqueous secretion by
Glaucoma
Ocular irritation
betaxolol,
inhibitory action on beta
Bronchospasm
levobunolol
adrenoreceptors in the
Bradycardia
cilliary body.
Nightmares
Exacerbation of
hear failure
Muscarinic
Pilocarpine (also
Increase aqueous outflow via
Glaucoma
Ocular: Misosis
(parasympath
a differential for
trabecular meshwork by
(reduced vision in
etic)
bilateral
ciliary muscle contraction
the presence of a
simulates .
constricted
cataract) spasm of
pupils!)
accommodation,
brow ache
Systemic: Swaeting,
bradycardia, GI
disturbance
Alpha2Brimonidine,
Reduces aqueos secretion by
Glaucoma
Ocular: Iris
stimulants
Apraclonidine
selective stimulation of
darkening,
Topical
alpha2 and adrenocrecptors
conjunctival
in the ciliary body increase
hyperaemia,
outflow by the uveoscleral
eyelash growth.
route
Systemic: bitter
taste, asthma.
Carbonic
Acetazolamide
Reduce aqueous secretion by
Glaucoma
Ocular route:
Anhydrase
(systemic)
the cilliary body
irritation and allergy
Inhibitors
Dorzolamide,
Systemic route:
Brinzolamide
Malaise,
paraesthesia, urea
and electrolye
disturbance,
aplastic anaemia
Mydriatics and cycloplegics ( Used for retinal examination and objective refraction (retinoscopy)
Antimuscarini
Tropicanamide,
Eye dilation for exam Inhibit muscarinic receptors
cs
cyclopentolate,
of parasympathetic nervous
atropine.
system to paralyse papillary
sphincter and ciliary muscle.
Alphastimulant
Phenylephrine
hyrpmellose,
polyvinyl alcohol,
liquid paraffin
Ant-Inflammatory Agents. Most important
immnosuppressants
Corticosteroid Prednisolone,
s
betamethasone,
dexamethasone
Dry eye
Antihistamines
Cromoglicate,
nedocromil,
lodoxamide.
Topical:
Antazoline,
azelastine,
levocabastine.
Ocular: Allergy,
blurred vision
drugs are corticosteroids, a Variety of other drugs are available including systemic
Suppress
Inflammation
Suppresion of broad
spectrum of inflammatory
processes (see
corticosteroids)
Mast cell
stabilisers
Ocular: Blurred
vision, glare, angle
closure glaucoma.
Systemic:
Tachycardia, dry
mouth, confusion,
tremor.
Ocular: Blurred
vision, glare, angle
closure, glaucoma,
conjunctival
blanching.
Systemic
hypertension
Allergy
Allergy
Ocular: Glaucoma
(especially with
local
administration),
cataract (especially
prolonged systemic
use) exacerbation
of some
infections !!! e.g.
herpes simplex.
Systemic: Negligible
with topical use,
common and varied
with systemic
administration.
Occular: Irritation
Occular route:
Irritation
Sytemic route:
Drowsiness
Systemic
(chlorphenamine,
terfendaine,
cetirisine)
NSAIDS
Topical:
Eye inflammation
(ketorolac,
diclofenac,
fluribiprofen)
Anti-Infective agents: Topically applied antibacterial and antiviral
and antiparastic agents is much less frequent.
Antibacterials
Topical:
Bacterial Infection
Chloramphenicol,
gentamicin,
ciprofloxacin,
Neomycin, fusidic
acid.
Occassionally
intra-ocular,
systemic
Antivirals
Aciclovir, topical
Herpes simplex,
or systemic
zoster
Modulate prostaglandin
production.
Systemic: Peptic
ulceration, asthma.
Ocular: blurred
vision, corneal
toxicity
Systemic: Rashes:
kidney, liver and
other effects may
occur with systemic
use.
Local Anaesthetics: Major uses are to relieve pain and thereby assist with clinical examination and the facilitation of surgical
anaesthesia
Local
Topical or periBlock conduction along the
Clinical exam
Ocular: Irritation,
anaesthesia
ocular injection.
nerve fibres
corneal toxicicty.
Oxyburprocaine,
Systemic: generally
proxymetacaine.
accidental
Tetracaine,
intravascular or
lidocaine.
intrathecal
(cerebrospinal fluid)
injection. During
surgical
anaesthesia,
cardiac
arrythmmias,
respiratory
depression
Botulinum toxin: Used in the management of certain ocular motility disorders amd blepharospasm, and to induce ptosis for
corneal protection
Botulinum
Injection at site of
Prevents release of the
Motility disorder
Dependant on
toxin
Migraine
Pizotifen
Sumatriptan
Acute
Migraine
Methysergide
Long term
migraine
Urinary Tract
Infection
Trimethoprim
action
neuro-transmitter
acetycholine at
neuromuscular junctions
treatment sitee.e.g
unwanted ptosis or
double vision
Serotonin
Antagonist
5HT
Serotonin
Antagonist
5HT
Serotonin
Antagonist
5HT
Migraine
Migraine
Migraine
E.coli, proteus,
saprophiticus.
UTI
Amoxicillin
UTI
NOT used in
pregnancy
Use nitrofurentoin
instead or
amoxicillin
Used in pregnancy
Diazoxide
Blocks insulin release
Insulinoma
Teriparatide
PTH
analogue
Hypocalaemia
Corticosteroids Release of cortisol is controlled by negative feedback mechanism involving the hypothalamus and anterior
pitruitary. Low plasms cortisol levels result in release of ACTH which stimulates cortisol synthesis and release by activating
Adenylate cyclise. cAMP then activates protein kinase A which phosphorylates and inceases the activity of cholesterylester
hydrolase, the rate limiting step in steroid synthesis. Aldosterone release is affected by ACTH but other factors (renin
angiotensin are more important.
Steroids are examples of gene active hormones. Steroid diffuses into cells where it binds to cytoplasmic glucocorticoid
receptors. IN the absence of cortisol the receptor is inactivated by a heat shock protein. Cortisol triggers the release of hsp90
and the activated receptor enteres the nucleus where it stimulates the synthesis of proteins, which then produce the
characteristic actions of the hormone.
Corticotrophin is prcessed from a large molecular weight precursor pro opiomelanocortin (POMC) precent in the corticotroph
cells of the adenohypophysis; its main action is tto stimulate the synthesis an release of cortisol. POMC also contains the
sequences for B lipoprotein (B-LPH) and B-endorphin, which are co comittantly release into the blood. Corticotrophin is also
believed to sensitize the zone glomerulosa to other stimuli which cause aldosterone release.
Glucocorticoids:- Mechanism of actionCortisol and synthetic glucocorticoids diffuse into target cells and binds to a cytoplasmic glucocorticoid receptor that belongs to
the superfamily of steroid thyroid and retinoid receptors. The activated receptor-glucocorticoid complex enters the nucleus and
binds to the steroid respsones elements on target DNA molecules. This either induces the synthesis of mRNA or represses the
genes inhibiting transcription factors e,g, NFkB for most clinical purposes, synthetic glucocoritcoids are used because they have
a higher affinity for the receptor are less rapidly inactivated and have little or no salt retaining properties.
Effects Glucorticosteroids are essential for life their most important function being facilitating the conversion of protein to
glycogen. They inhibit protein synthesis and stimulate protein catabolism to amino acids. Gluconeogenesis glycogen deposition
and glucose release from the liver are stimulated, but peripheral glucose uptake is inhibited. During fasting they are essential
for the anti-flamm effects of NSIADS. Inhibition of COX 1 is responsible for GI problems. Most current NSAIDS are COX 1
inhibitors, but selective COX 2 are on the market (Celecoxib, eterocoxib, valdecoxib) are selective COX 2 inhibitors incidence of
gastric perforation obstruction and bleeding is reduced by at least 50%.
Aspirin is long standing NSAID and anti analgesic
Paracetamol is just analgesic