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Class III Amiodarone, • AF, AT, AVRT, Block K+ channels so prolong • Amiodarone : GI
Bretylium, Sotalol AVNRT, WPW, NSVT the duration of the action disturbances.
(Beta blocker with potential. Corneal
class III microdeposits,
properties) throtoxicosis,
photosensitivity
Class IV Calcium channel • AVRT, AVNRT, Block Ca2+ channels – acts • Flushing, headache
blockers (see Paroxysms predominantly on the AVN • P.oedema
above also) and affect the plateau phase • Phenyalkylamines –
of the action potential. can worsen heart
failure
• Gynaecomastia
• Impotence
Digoxin • AF Not strictly antiarrythmic – • Intracellular Ca2+
• Atrial Flutter indirect actions on the Action overload –
potential through stimulation junctional escape
of the vagus nerve: beats, junctional
↓ automaticity of the SA tachycardia,
node which slows sinus rate ventricular ectopic
↑ refractory period of the AVN beats, VT.
which ↓ AV conduction • Increased vagal
activity can cause
AT with 2:1 AVN
block
• GI disturbances
• Neurological
disturbances
• Gynaecomastia
Adenosine • Supraventricular Potent effect on SA node • Bradycardia and AV
arrythmias producing sinus bradycardia. block
Slows impulse conduction • Malaise, flushing,
through the AVN but has no headache chest
effect on conduction in the pain, bronchospasm
ventricles.
Atropine • Sinus bradycardia Inhibits effect of the vagus • Rhythm
• AV block nerve on the heart which disturbances
• Cardiopulmonary ↑ rate of firing of SA node • Constipation
resuscitation ↑ conduction through the • Reduced Bronchial
AVN via blockade of secretions
muscarinic M2 receptors.
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 • IV for Simple solution of insulin
hyperglycaemic (onset 30 mins, peak
emergencies. activities 2-4hrs, subsides by
• Subcutaneous 8hrs)
injection If IV effects only last 30
minutes.
Insulin lispro Humalog and • Blood glucose Insulin analogues have a • Hypoglycaemia
and Insulin Novorapid control faster onset and shorter
aspart (Rapid action than soluble insulin. • Insulin auto
Acting) This is because they do not antibodies
self associate to form • Lipohypertrophy
dimmers.
Onset 20-30 minutes Peak
action 1-2 hrs Duration 3-4
hrs
Intermediate and Long Acting Insulin
(duration of action between 16-35 hours)
Semilente • Blood glucose Suspension of amorphous • Hypoglycaemia
(amorphous control insulin zinc.
insulin zinc)
Lente Humulin L or • Blood glucose conrol Mixture of amorphous insulin • Hypoglycaemia
Monotard zinc (30%) and insulin zinc
crystals (70%), the latter
prolonging the duration of
the preparation Onset of
action (2-4 hours). Peak
action (6-12hrs) (Duration 20
hrs)
Isophane Insulatard • A complex of protamine and • Hypoglycaemia
Insulin (NPH) insulin. The mixture is such
that no free binding sites
remain on the proatmine.
After injection, proteolytic
enzymes degrade the
protamine and the insulin is
absorbed. The duration of
NPH is similar to that of
Lente
Onset of action (30-90
mins) Peak action (4-6 hrs)
Duration action (8-16 hrs)
Biphasic fixed Human mixed • Contain various proportions • Hypglycaemia
mixtures (short- and of soluble isophane insulin
intermediate- (e.g. 30% soluble and 70%
acting) insulins: isophane) The soluble
These include component gives rapid onset
Humulin 20/80, and the isophane insulin
Humulin 30/70, prolongs the action.
Humulin 50/50, A pre-mixed short and
Mixtard 20/80, intermediate-acting insulin
Mixtard 30/70, will start to work half an hour
and Mixtard after being injected, peak at
50/50. 1-12 hours and last for 16-24
hours.
Human mixed The ultra-short acting
insulin analogues insulins lispro and aspart are
(with ultra- also available in a biphasic
short and form which retains the rapid
intermediate- onset of action (about 15
acting minutes) but has a duration
properties): of action similar to that of
These include intermediate-acting isophane
Humalog Mix25 insulins.
(insulin lispro)
and NovoMix 30
(insulin aspart).
Sulphonyreas Glipizide (short • Type II diabetes These drugs are indicated in • GI disturbance
half life) (people with ideal patients (especially those • Rashes
Glicazide (short weight) near their ideal weight) in • Hypoglycaemia
half life) whom diet fails to control the • Hypoglycaemic
Glibenclamide hyperglycaemia. In about coma
(longer duration 30% control is not achieved • Contraindicated in
of action) by these drugs. They severe
Tolbutamide. stimulate insulin release hyperglycaemia,
from the pancreatic islets surgery and major
and so patient must have illness
partially functional B-cells for
these drugs to be of use.
Glitazones Rosiglitazone and • Type II diabetes Slow onset maximum effect • Weight gain
Pioglitazone given alone or in 1-2 months of treatment. • Fluid retention
combination with Reduce hepatic glucose • Contraindicated in
metofrmin or output and increase pregnancy
sulphonyreas in absorption into the
patients who cannot peripheral tissues.
tolerate metformin Triglycerides decline and LDL
or sulphonyreas is also reduced.
combinations. Drugs increase sensitivity to
insulin by binding to the
nuclear peroxisome
proliferator activated
receptor gamma (PPAR-y)
and by derepression,
increase transcription of
insulin sensitive genes.
NSAIDS inhibit COX and inihibit prostaglandin synthesis. COX exists in tissue as constitiutive isoform (COX-1) but at sites of
inflammation cytokines stimulate the induction of a second isoform (COX-2) Inhibition of of COX-2 is thought to be responsible
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
• •
• •