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ACE inhibitors Ramipril, Lisinopril Hypertension Block ATIATII by binding to the site Hypotension
Heart Failure on the enzyme that normally Dry cough (increased
Post MI accommodates the terminal leucine of bradykinin)
ATI. Inhibits vasoconstriction. Renal failure in pts with
bilateral renal stenosis
Beta-Blockers Atenolol, Propanolol Hypertension block -adrenergic receptors inhibiting the Provocation of asthma,
Angina effects of adrenaline and nonadrenaline. heart failure.
Arrhythmias 1 (heart) blockage decreases HR and Cold hands
Stable heart failure contractility, 2 (bronchial and vascular Bradycardia - fatigue
smooth muscle) blockage causes
vasodilation.
Antiplatelet agents
Asprin Prevention and treatment of Irreversibly inhibits COX and so stops Haemorrhage
MI and stroke. synthesis of Thromboxane A2 from
Arachidonic Acid which leads to
platelet aggregation.
Clopidogrel Prevention and treatment of Inhibits activation of the glycoprotein Haemorrhage
MI and stroke. IIb/IIIa receptor on the surface of
platelets which is required for
aggregation to occur.
Anticoagulants
Warfarin Prophylaxis+treatment DVT, Blocks reduction of Vit. K epoxide Haemorrhage
PE necessary for synthesis of factors II, VII,
Prophylaxis of embolization IX and X.
in AF, Rheumatic disease +
prosthetic valves.
Heparin Treatment of DVT, PE. Activates antithrombin III, which limits Haemorrhage
Prophylaxis of DVT/PE post blood clotting by inactivating thrombin
op. and factor X.
MI.
Statins Atorvastatin, Prevention of cardiovascular Reversibly inhibit enzyme HMG CoA Myopathy (muscle ache)
Simvastatin, Pravastatin disease reductase which catalyses the rate- Disturbed LFTs
limiting step in the synthesis of Abdominal pain
cholesterol:
HMG CoAmevalonic
acidcholesterol.
This in synthesis LDL receptors so
LDL levels.
Nitrates Glyceral trinitrate (GTN), Prophylaxis and Treatment Prodrugs – they decompose to form NO Postural hypotension
Isosorbide mononitrate of angina. which activates guanylyl cyclase, Tachycardia
LVF thereby cyclic guanosine Headache
monophosphate (cGMP). Protein kinase Flushing
G is activated and contractile proteins Dizziness
are phosphorylated. This all leads to
Dilation of vessels.
Potassium channel Nicorandil (only licensed Prophylaxis of angina Relaxation of smooth muscle and Headache
activators one) vasodilation.
Activates K+ channels of vascular
smooth muscle causing K+ to flow out of
cells causing hyperpolarization. This
therefore inhibits influx of Ca2+ and so
inhibits contraction.
Antiarrythmics
Class Ia Quinidine, VT Block Na2+ channels which increases GI disturbances
Disopyramide, WPW refractory period and in addition there is Hypotension
Procainamide a blockade of K+ channels which delays
repolarisation.
Class Ib Lignocaine, Mexiletine, Ventricular arrythmi, Block Na2+ channels but little effect on Nausea and Vomiting
Phenytoin especially VT refractory period as K+ channels not CNS toxicity
blocked. duration of the action Hypotension
potential. Bradycardia
Class Ic Flecainide Pre-excitation AF Marked Na2+ channel blockage CNS toxicity
cardioversion of refractory period, no effect on the Hypotension
paroxsms,AVNRT ,AVRT, duration of the action potential. Proarrythmogenic after
WPW, AF , AT , NSVT (non- recent MI – may increase
sustained VT) mortality
Class II Beta blockers (see Junctional tachyarrhythmias, rate of spontaneous depolarisation of Provocation of asthma,
above also) Paroxysmal events,AF, SA and AV nodal tissue heart failure.
Flutter, NSVT, SVT’s. conduction through AV node Cold hands
Class III Amiodarone, Bretylium, AF, AT, AVRT, AVNRT, Block K+ channels so prolong the Amiodarone : GI
Sotalol (Beta blocker WPW, NSVT duration of the action potential. disturbances. Corneal
with class III properties) microdeposits,
throtoxicosis,
photosensitivity
Class IV Calcium channel AVRT, AVNRT, Paroxysms Block Ca2+ channels – acts Flushing, headache
blockers (see above predominantly on the AVN and affect the P.oedema
also) plateau phase of the action potential. Phenyalkylamines – can
worsen heart failure
Gynaecomastia
Impotence
Digoxin AF Not strictly antiarrythmic – indirect Intracellular Ca2+ overload –
Atrial Flutter actions on the Action potential through junctional escape beats,
stimulation of the vagus nerve: junctional tachycardia,
automaticity of the SA node which ventricular ectopic beats,
slows sinus rate VT.
refractory period of the AVN which Increased vagal activity can
AV conduction cause AT with 2:1 AVN
block
GI disturbances
Neurological disturbances
Gynaecomastia
Adenosine Supraventricular arrythmias Potent effect on SA node producing Bradycardia and AV block
sinus bradycardia. Slows impulse Malaise, flushing, headache
conduction through the AVN but has no chest pain, bronchospasm
effect on conduction in the ventricles.
Atropine Sinus bradycardia Inhibits effect of the vagus nerve on the Rhythm disturbances
AV block heart which Constipation
Cardiopulmonary rate of firing of SA node Reduced Bronchial
resuscitation conduction through the AVN via secretions
blockade of 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 hyperglycaemic Simple solution of insulin (onset 30 mins,
emergencies. peak activities 2-4hrs, subsides by 8hrs)
Subcutaneous injection If IV effects only last 30 minutes.
Insulin lispro and Humalog and Novorapid Blood glucose control Insulin analogues have a faster onset Hypoglycaemia
Insulin aspart (Rapid and shorter action than soluble insulin. Insulin auto antibodies
Acting) This is because they do not self Lipohypertrophy
associate to form 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 (amorphous Blood glucose control Suspension of amorphous insulin zinc. Hypoglycaemia
insulin zinc)
Lente Humulin L or Monotard Blood glucose conrol Mixture of amorphous insulin zinc (30%) Hypoglycaemia
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 Insulin Insulatard A complex of protamine and insulin. The Hypoglycaemia
(NPH) 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 (short- Contain various proportions of soluble Hypglycaemia
mixtures and intermediate-acting) isophane insulin (e.g. 30% soluble and
insulins: These include 70% isophane) The soluble component
Humulin 20/80, Humulin gives rapid onset and the isophane
30/70, Humulin 50/50, insulin prolongs the action.
Mixtard 20/80, Mixtard A pre-mixed short and intermediate-
30/70, and Mixtard acting insulin will start to work half an
50/50. hour after being injected, peak at 1-12
hours and last for 16-24 hours.
Human mixed insulin The ultra-short acting insulins lispro and
analogues (with ultra- aspart are also available in a biphasic
short and intermediate- form which retains the rapid onset of
acting properties): These action (about 15 minutes) but has a
include Humalog Mix25 duration of action similar to that of
(insulin lispro) and intermediate-acting isophane insulins.
NovoMix 30 (insulin
aspart).
Sulphonyreas Glipizide (short half Type II diabetes (people with These drugs are indicated in patients GI disturbance
life) ideal weight) (especially those near their ideal weight) Rashes
Glicazide (short half life) in whom diet fails to control the Hypoglycaemia
Glibenclamide (longer hyperglycaemia. In about 30% control is Hypoglycaemic coma
duration of action) not achieved by these drugs. They Contraindicated in severe
Tolbutamide. stimulate insulin release from the hyperglycaemia, surgery
pancreatic islets and so patient must and major illness
have partially functional B-cells for these
drugs to be of use.
Glitazones Rosiglitazone and Type II diabetes given alone Slow onset maximum effect 1-2 months Weight gain
Pioglitazone or in combination with of treatment. Reduce hepatic glucose Fluid retention
metofrmin or sulphonyreas in output and increase absorption into the Contraindicated in
patients who cannot tolerate peripheral tissues. Triglycerides decline pregnancy
metformin or sulphonyreas and LDL 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