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DRUG EXAMPLES USES MECHANISM SIDE EFFECTS

ACE inhibitors Ramipril, Lisinopril  Hypertension Block ATIATII 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.

Calcium Channel Dihydropines –  Hypertension Vasodilation  Flushing, headache,


Blockers Amlodipine,  Angina block cellular entry of Ca+ by preventing  P.oedema
Phenyalkylamines -  Supraventricular arrhythmia opening of voltage-gated L-type and T-  Phenyalkylamines – can
Verapamil, – (Phenylalkylamines only) type calcium channels worsen heart failure
Benzthiazepines -  Gynaecomastia
Diltiazem  Impotence
Thiazide Diuretics Bendrofluazide,  Hypertension increase water excretion by decreasing  Hypokalaemia
hydrochlorothiazide  Combined with loop for Heart reabsorption of Na+ and Cl- in the distal  Hyponatraemia
Failure tubule by binding to the Cl- site of the  Hypotension
electroneutral Na+/Cl- co-transport  Gout
system and inhibiting its action causing a  Type II DM
decrease in blood volume, venous return
and CO
Loop Diuretics Frusemide, Bumetanide  Hypertension (but less Block Na+ resorption in ascending loop of  Hypokalaemia
effective than thiazides – Henle – diuretic effect.  Hyponatraemia
used when renal impairment  Hypotension
or resistant to multiple drug  Gout
Tx)
 Heart Failure
Potassium-sparing Spironolactone,  Secondary Hypertension Blocks action of aldosterone in distal  Hypokalaemia
diuretics Amiloride  Severe heart Failure convoluted tubule – diuretic effect  Hyponatraemia
 Abdominal discomfort
Angiotensin II receptor Losarten, Valsarten  Hypertension Vasodilation – by inhibition at the  Usually mild
antagonists  Alternative to ACE inhibitor in angiotensin II receptor  No cough like in ACE
heart failure inhibitors
Alpha-adrenoreceptor Doxazosin, Prazosin  Hypertension (in addition to Reduces peripheral resistance by  Postural Hypotension
antagonists other hypertensives) inhibiting 1-adrenoreceptor-mediated  Dizziness
vasoconstriction.
Fibrinolytics Streptokinase  Thrombolysis – Acute MI, Forms a complex with, and activates,  Nausea/vomiting
stroke, PE plasminogen into plasmin.  Bleeding

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 CoAmevalonic
acidcholesterol.
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).

Ultralente Humulin UL A suspension of poorly soluble insulin  Hypoglycaemia


Ultratard 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)
Insulin glargine Lantus Is soluble at acid pH. It has a long  Hyoglycaemia
peakless activity (11-12 hrs) and is given
once a day.
Oral Anti Diabetic Drugs
Tablets are introduced when metabolic control cannot be obtained by diet and lifestyle changes alone. Choice depends on individuals characteristics. Patients with baseline
Hb1A1c 9% are les likely to achieve target HbA1c with monotherapy. Drug of choice started at low dose, dose is increased, additional drugs are introduces in combination therapy
to maximum of 2-3 drugs. Insulin is usually introduced in combination with metformin.
Bigunides Metformin  Type 2 diabetes The exact mechanism of action of  Lactic acidosis rare and
Only diabetic drug that  PCOS metformin is uncertain. It appears to act limited to those with
reduces cardiovascular  Non Alcoholic fatty liver mainly by reducing hepatic impaired liver of kidney
risks. disease gluconeogenesis, it also decreases function.
It reduces weight. absorption of glucose from the  GI upset diarrhoea,
gastrointestinal tract and increases vomiting cramps.
insulin sensitivity by increasing
peripheral utilization of glucose.]
Evidence suggests that increased
peripheral utilization of glucose may be
due to improved insulin binding to insulin
receptors since metformin is not
effective in patients who no longer have
any residual insulin production.The
'average' person with type 2 diabetes
has three times the normal rate of
gluconeogenesis; metformin treatment
reduces this by over one third.
Metformin stimulates the hepatic
enzyme AMP-activated protein kinase
(AMPK), which plays an important role in
the metabolism of fats and glucose.
Causing weight loss. The molecular
targets with which metformin directly
interacts remain elusive.
Metformin is not metabolized, rather it is
primarily excreted in the urine with an
elimination half-life of 6.2 hours

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.

a- Glucosidase Acarbose  Type II diabetes Inhibits intestinal a-glycosidases,  Flautlence


inhibitors delaying the digestion of starch and  Diarrhoea
sucrose. It is taken with meals and  Abdominal Pain
lowers the post prandial increase of
blood gluocose.
Prolactinomas- oligomenorrhoea, amenoffhoea, galactorrhea, infertility, loss of libido, erectile dysfunction, osteoporosis. TRH stimulates prolactin, Dopamine inhibits it.
Dopamine agonist Bromocriptine (ergot  Prolactinoma Stimulates dopamine receptors in the  Nausea
drugs derivative)  Acromegaly brain.  Psyhchiatric Symptoms
Cabergoline  Hypogandism  Postural Hypotension
 Galactorrhea  Fibrotic changes which can
lead to valvular heart
disease.
Acromegaly Over secretion of GH =gigantism before puberty, acromegaly after puberty. (growth of hands feet, tightening of rings)
Somatostatin Somatuline Autogel  Acromegaly Somatostatin analogue. Inhibits the  Gallstones
analogues Sandostatin LAR production of GH.  Conratindicated in liver and
Ocreotide kidney failure, diabetes
mellitus, Insulinoma.
Diabetes Insipidus (no ADH produced so leads to excretion of large volumes of isotonic water)
ADH analogue Desmopressin (nasal  Diabetes Insipidus Desmopressin is preferred to  Water retention
spray, tablets, or vasopressin because it is a longer acting  Hyponatremia
subcutaneous injection) analogue. Make sure to reduce fluid  Contraindicated in heart
intake. failure, people using
diuretics for other
conditions. Alcoholics
Hypothyroidism tiredness and lethargy are the most common symptoms. Depression of basal metabolic rate, appetite and cardiac output. Low output heart failure might occur.
Skin is dry. Thyroid deprivation in early life leads to dwarfism and cretinism.
Thyroxine Levothyroxine  Hypothyroidism Administered orally is the treatment of  Concomitant conditions
choice. Synthetic T4 is the sodium salt of worsened by thyroxine
levothyroxine (L-thryoxine). Its effects therapy. Heart disease,
are delayed until the plasma protein and heart failure, infarction,
tissue binding sites are occupied. angina, chronic lung
Treatment is assessed by monitoring disease, breathlessness,
TSH levels, which fall to normal when adrenal disease. Due to
optimum dose is achieved. Daily dose increase in oxygen demand
100 and 150ug best take on waking. of most tissues as well as
myocardium
Liothyronine  Hypothyrioidism Is the sodium salt of T3 and because it  See above
is less protein bound, it acts more
quickly than T4. The main use of T3 is in
hypothyroid coma, when it is given with
hydrocortisone by IV injection.
Hyperthyroidism basal metabolic rate is increased, causing heat intolerance, arrthymias and increased appetite with weight loss. Skin is warm and moist. Tachycardia sweating
and tremor. Angina and high output failure may occure. Upper eyelids are retracted. Treatment also includeds beta blockers discussed above (Propranalol or atenolol)
Antithyroids Carbimazole  Hyperthyroidism Rapidly converted to methimazole in  Rashes
vivo  Agranulocytosis
Once daily doses, 40mg for 1 month,  Patients should report a
then 30mg for 1 month, 20mg for 1 sore throat!
month and then 10 mg daily until
reassessed.. Onset of action 3-4 weeks
Thionamides  Hyperthyroidism Possess a thiocarbamide group that is  ? immunosuppressive
essential for their activity. They prevent
the synthesis of thyroid hormones by
competitively inhibiting the peroxidise
catalysed reactions necessary for iodine
organification. They also block the
coupling of iodotyrosine especially
diiodothyronine formation. Onset of
action 3-4 weeks
Propylthiouracil  Hyperthyroidism Reserved for patients intolerant of  ?immunosupressive
carbimazole. Also inhibits the peripheral
deiodination of t4
Iodides  Hyperthyroidism Have poorly understood actions on the  Skin rashes
thyroid. They inhibit organification and  Nausea
and hormone release. In addition iodide  Vomiting
decreases the size and vascularity of the  Allergic reaction.
hyperplastic gland, effects which are
useful in preparation of patients for
thyroidectomy. They inhibit hormone
release quickly (2-7 days) is a valuabe
treatment for thyrotoxic crisis. Cannot be
used in long term because its antithyroid
action tends to diminish.
Primary Hypoadrenalism: Addisons disease Normally! Glucocorticoids mainly cortisol are produced in the cells of the zona fasiculata and zona reticularis. The release of cortisol is
controlled by negative feedback mechanism involving the hypothalamus and anterior pituitary. Low plasma cortisol levels results in the release of ACTH. Which stimulates coritsol
synthesis and release by activiating adenlyl cyclise. Cyclic adenosine monophosphate (cAMP) then activates protein kinase A, which phoshoporylates and increases the activity of
cholesterylester hydrolase, the rate limiting step in steroid synthesis. Alodosterone release is effected by ACTH, but Renin release is more important influence. The steroids are
examples of gene active hormones. The steroid diffuses into the cells. In the absence of cortisol the receptor is inactivated by a heat shot protein (hsp 90). Cortisol triggers the
release of hsp90 and the activated receptor SR enters the nucleus where it stimulates or inhibits the production or proteins, which then produce the characteristic actions of the
hormone.
Coritcothrophin releasing hormone (CRH) is a 41 amino acid polypeptide whose action is enhanced by arginine avasopressin (ADH). It is produced in the hypothalamus and
reaches the adenopophysis in the hypothalamus-hypophsyial portal system where it stimulates the production of corticotrophin.
ACTH is process from large molecular weight precursor, pro-opiomelanocortin (POMC) present in corticotroph cells of the adenohypophosis, its main action is to stimulate the
synthesis and release of cortisol.
Cortisol Hydrocortisone  Addisons Immediate management. If acutely sick!  Moon face
Take blood cortisol glucose urea and  Striae
electrolytes. Give hydrocortisone 100mg  Fat redistribution
as IV bolus. Give saline infusion litre  Hirsutsim
initially over 4-6 hours. Correct  Infection
hypoglycaemia iwth IV bolus of 20%  Proximal muscle wasting
glucose.
 Bruising
Continue with with IM hydrocortisone
100mg 6 hourly.
Long term
Hydrocortisone orally 10mg on waking,
5mg at lunch and evening (dose varies)
Fludrocortisone 0.1-0.2mg per day.
Synthetic Aldosterone Fludrocortisone  Addisons Synthetic mineralcorticoid derivative of  Hypertension
aldosterone. Plasme rennin acitivity  Oedema
should be measured 2 hours after the  Peptic ulcers
flurdrocortisone dose and maintained in  Mood changes
the normal range.  GI upset
 Glaucoma
Cushings Syndrome Excess production of cortisol
Ketoconazole  Cushings Well absorbed orally, wide spectrum anti  Hepatic necrosis
 Anti fungal fungal drug which has adrenal  Adrenal suppression
suppression effects
Metirapone  Cushings Metyrapone blocks cortisol synthesis by  Nausea vomiting,
inhibiting steroid 11β-hydroxylase. abdominal cramping pain.
Mitotane  Cushings Unknown mechanism of action but  Dizzyness, drowsyness
 Adrenal adenoma inhibits adrenal steroidal action nausea and vomiting.
Hyperparathyroidism and Malignancy account for 90% of Hypercalcaemia
Rehydration IV Saline  Hypercalcaemia Hydration must be maintained with IV  Hypernaetremia
intravenous saline. This will prevent
severe hypercalcaemia. Once volume
status is normal use bisphosphonates
Bisphosphonates Alendronate  Hypercalcaemia Bind to hyrdoxyapatite crystals and  GI upset, Erosion of
Etidronate reduce bone resorption. Oesophagus
Hypocalaemia Commonest cause is Vit D deficiency
Calcium Supplements Calcica  Hypocalaemia  Hypercalcaemia
Osteocare  Stomach pain
 Diarrhoea
Vitamin D analogue Ergocalciferol Vit D2  Hypocalcaemia Vitamin D analogues allow absorption of  Hypercalcaemia
Cholecalciferol Vit D3  Vit D deficiency calcium from the gut.
Alfacalcidol 1-
hydroxyvitamin D
Calcitriol 1,25
Dihydroxy D
Recombinant PTH Teriparatide  Hypocalcaemia Stimulates bones resorption, Kindey to  Dizzyness
analogue  Hypoparathyriodism re absorb calcium, stimulates production  Leg Cramps
of 1.25 Dehydroxyvit D at kidney.  Nausea
Phaeochromocytoma Neoplasm of the adrenal medulla. 10% are malignant, 10% are extra-adrenal, 10% are bilateral, 10% are familial. Blockage of adreno receptors must be
started first.
a-adrenoreceptor Phenoxybenzamine  Tumours of adrenal medulla An irreversible antagonist is used to  Reflex tachycardia
antagonist Labetalol block the a-effects of the large amounts
Doxazosin of catecholamines from tumours of the
Phentolamine adrenal medulla.
Prazosin
Tamsulosin
Terazosin

b-blockers Atenolol (see above)  


Conns excess production of aldesterone
Aldosterone receptor Spironolactone (see  Conns Blocks the binding of aldosterone to its  Severe Hyperkaleamia
blockers above)  Liver disease with ascites receptor and increases the excretion of  Painful Gyanocamastia
Eplernone Na+ and decreases the electrically
coupled K+ secretion.
Postassium Sparing Amiloride  Potassium sparing diuretic Decrease the luminal membrane Na+  Severe Hyperkalaemia
Diuretic Triamterene  Conns permeability in the distal nephron by
combining with Na+ channels and
blocking them 1:1 basis. This increases
Na+ (Cl- and H2O) excretion and
decreases K+ excretion.
Zero Order Kinetics 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 Epilepsy Lamatrogine  Lamatrogine and Valpraote have similar  Lamatrogine – Blurred
Sodium Valproate mech of action as Phenytoins discussed vision dizziness and
below. Valproate also seems to in drowsyness. Serious skin
increase GABAergi central inhibition reactions can occur
mechanisms that may involve especially in children.
stimulation of glutamic acid  Valproate - Nausea, weight
decarboxylase activity and/ or inhibition gain, bleeding tendencies
of GABA-T activity. and transient hair loss). The
main disadvantage is that
occasional idiosyncractic
reactions cause sever or
fatal hepatic failiure.
Focal Epilepsy Carbamazepine  Phenytoins anticonvulsant action is  Carbamazepine is
Phenytoin probably a result of its ability to prevent metabolised in the liver to
high frequency repetitive activity. carbamzepine-10,11-
Phenytoin binds prerentially to epoxide, an active
inactivated (closed) Na+ channels metabolite that partly
stabilizing them in the inactivated state contributes to both its anti-
and preventing them from returning to convulsant action and
the resting closed state which they must neurotoxicity. In contrast to
do before they can open again. High phenytion there is a linear
freuquency repetitive depolarisation increase in serum
increases the proportion of Na+ concentration with dosage.
channels in the inactivated state and, Mild neurotoxic effects are
because these are susceptible to common (nausea dizziness
blockade by phenytoin, the Na+ is drowsyness, blurred vision
progressively reduced until it is and ataxia) Agranulocytosis
eventually insufficient to evoke and is a rarer idyiosyncratic
action potential. Neruonal transmission reaction.
at normal frequencies is relatively  Phenytoin is hyroxylated in
unaffected by phenytoin because a the liver by a saturable
smaller portion of the Na+ channels are enzyme system. The rate of
in the inactivated state. Carbamazepine, metabolism varies greatly in
lamotrigine, valproate, and topiramate. patients. And up to 20 days
Have similar actions on neuronal Na+ maybe required for the
channels. 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 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.
Absence Epilepsy in Ethosuximide  Absence seizures involve oscillatory  Ethosuximide- Nausea
Children Sodium Valproate neuronal activity between the thalamus vomiting.
and the cerebral cortex. This oscillation
involves (T-type) Ca2+ channels in the
thalamic neurones, which produce low
threshold spikes and allow the cells to fie
in bursts. Drugs (Ethosuximide and
Valproate) that control absences
reduced this Ca2+ current dampening
the thalmacortical osciallations that are
critical in the generation of absece
seizures.
Parkinsons – Main pathology is the extensive degeneration of the dopiminergic nigrostriatal tract, but the cause of the degeneration is usually unknown. Replacement therapy
alone is not possible in parkinsons because the dopamine does not pass the blood brain barrier. However its precursor levodopa (L-dopa), does penetrate the brain where it is
decarboxylated to dopamine. Orally administered, levodopa is largely metabolized outside the brain and so it is given with a selective extracerebral decarboxylase inhibitor
(carbidopa or benserazide). Some of the peripheral side effects of dopaminergic drugs can be reduced with domperidone, a dopamine antagonist that does not penetrate the
brain. Inhibition of the drug monoamine oxidase B (MAOb) with selegilene potentiates the actions of levodopa. Anti-muscarincs are used for the tremor that occurs with
parkinsons.
Levodopa Sinemat  Parkinsons Levodopa is the immediate precursos of  Nausea and vomiting
Madopar dopamine and is able to penetrate the caused by stimulation of the
Both these drugs come brain where it is converted to dopamine. CTZ.
with extracerebral The site of the decarboyxlation is  Psych effects vivid dreams,
decarboxylase inhibitors) uncertain, but as dopa decarboxylase is hallucinations, psychotic
no rate limiting there maybe sufficient states and confusion.
enzyme in the remaining dopaminergic  Postural hypotension is
nerve terminals. Another possibility is common.
that the conversion occurs in nor  Dyskinesias (jerky or dance
adrenergic or seratonergic terminals. like movement) are an
Because the de-carboxylase activity in important adverse effect.
these neurones is not specific.  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.
Dopamine Receptor Bromocriptine (ergot  Parkinsons Dopamine agonists have no advantage  Nausea, psychiatric
Agonists derivative)  Prolactinomas over levopdopa and the adverse effects symptoms, postural
Ropinirole (non ergot are similar. hypotension.
derivative) Used with young patients, in particular  Pulmonary fibrosis and
Apomorphine (very who are given a dopamine agonist as retroperitoneal fibrosis.
powerful given by initial therapy (sometimes together with  Apomorphine (highly
parenteral selegeline). This strategy may slow the emetogenic) domperidone
administration) development of dyskinesias but only should be given before
50% of patients show any beneficial treatment started.
response to monotherapy with dopamine
agonists.
When patients on levodopa therapy start
to show deterioiration dopamine
agonists are often added to try and
reduce the off periods.
Pre Synaptic Re- Amantadine  Parkinsons Potentiates dopamine by preventing re-  Dizzyness, Loss of co-
Uptake inhibitor uptake in the pre-synaptic terminals. ordindation, inability to
Moderate effect but toleranc soon sleep, nausea, nervousness
develops
Monamine oxidase Selegiline  Parkinsons Inhibits monoamine oxidase type B  Nausea
inhibitor type B (MAO- (MAO-B) there by increasing dopamine.  Heartburn
B) This is done by reducing the metabolism  Dry mouth
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 inhibitors Entacapone  Parkinsons Inhibbits catechol-O-methltransferase  Drowsyness
Benzarazide (COMT) and prevents peripheral  Dizzyness
conversion of Levodopa to (inactive) 3-  Stomach upset
O-methyldopa. It increases the plasma  Diarrhoea
half life of levodopa and increases its
action.
Antimuscarinics Benzetropine  Parkinsons Produce a modest iimprovement in the  Dry mouth
Procyclidine early stages of parkison’s disease, but  Urinary retention and
Orphenadrine the akinesia responsible for most of the constipation.
Benzhexol functional disability responds least well.  Effect memory and
concentration.
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  Myaesthenia gravis Most widely used drug; it has a duration  Overdose causes a
acetycholinesterase of about 3-5 hours. Patients response cholinergic crisis with
will determine the dose required. Great severe weakness. Colic and
symptomatic drug but does not alter the diarrhoea may occur.
natural history of the disease.
Motor neurone disease
Riluzole Rilutek  MND Used to treat amyoptrophic lateral  Nausea
sclerosis. Delays the onset of ventilator  Fatigue
dependence or tracheostomy by 2  Hepatitis
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)  Guillen Barres Either high-dose intravenous  Hepatitis
immunoglobulins immunoglobulins (IVIg) at 400mg/kg for  Renal failure
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,  Glaucoma Reduce aqueous secretion by inhibitory  Ocular irritation
betaxolol, levobunolol action on beta adrenoreceptors in the  Bronchospasm
cilliary body.  Bradycardia
 Nightmares
 Exacerbation of hear failure
Muscarinic Pilocarpine (also a  Glaucoma Increase aqueous outflow via trabecular  Ocular: Misosis (reduced
(parasympathetic) differential for bilateral meshwork by ciliary muscle contraction vision in the presence of a
simulates . constricted pupils!) cataract) spasm of
accommodation, brow ache
 Systemic: Swaeting,
bradycardia, GI disturbance
Alpha2-stimulants Brimonidine,  Glaucoma Reduces aqueos secretion by selective  Ocular: Iris darkening,
Topical Apraclonidine stimulation of alpha2 and conjunctival hyperaemia,
adrenocrecptors in the ciliary body eyelash growth.
increase outflow by the uveoscleral route  Systemic: bitter taste,
asthma.
Carbonic Anhydrase Acetazolamide  Glaucoma Reduce aqueous secretion by the cilliary  Ocular route: irritation and
Inhibitors (systemic) body allergy
Dorzolamide,  Systemic route: Malaise,
Brinzolamide paraesthesia, urea and
electrolye disturbance,
aplastic anaemia
Mydriatics and cycloplegics – ( Used for retinal examination and objective refraction (retinoscopy)
Antimuscarinics Tropicanamide,  Eye dilation for exam Inhibit muscarinic receptors of  Ocular: Blurred vision,
cyclopentolate, atropine. parasympathetic nervous system to glare, angle closure
paralyse papillary sphincter and ciliary glaucoma.
muscle.  Systemic: Tachycardia, dry
mouth, confusion, tremor.
Alpha-stimulant Phenylephrine  Eye dilation for exam Stimulates dilator muscle of the pupil no  Ocular: Blurred vision,
cycloplegic effect. glare, angle closure,
glaucoma, conjunctival
blanching.
 Systemic hypertension
Lubricants – There are a wide range
Carbomers,  Dry eye Exact mechanism depends on the agent  Ocular: Allergy, blurred
hyrpmellose, polyvinyl vision
alcohol, liquid paraffin
Ant-Inflammatory Agents. Most important drugs are corticosteroids, a Variety of other drugs are available including systemic immnosuppressants
Corticosteroids Prednisolone,  Suppress Inflammation Suppresion of broad spectrum of  Ocular: Glaucoma
betamethasone, inflammatory processes (see (especially with local
dexamethasone corticosteroids) 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.
Mast cell stabilisers Cromoglicate,  Allergy Stabilise mast cells  Occular: Irritation
nedocromil, lodoxamide.
Anti-histamines Topical: Antazoline,  Allergy Block histamine receptor  Occular route: Irritation
azelastine,  Sytemic route: Drowsiness
levocabastine.
Systemic
(chlorphenamine,
terfendaine, cetirisine)
NSAIDS Topical: (ketorolac,  Eye inflammation Modulate prostaglandin production.  Systemic: Peptic ulceration,
diclofenac, fluribiprofen) asthma.
Anti-Infective agents: Topically applied antibacterial and antiviral drugs are very commonly prescribed. The use of antifungal and antiparastic agents is much less frequent.
Antibacterials Topical:  Bacterial Infection Range of activities and specificities  Vary with agent
Chloramphenicol,  Ocular: allergy; corneal
gentamicin, toxicity common with
ciprofloxacin, intensive use.
Neomycin, fusidic acid.  Systemic: generally only
Occassionally intra- with systemic use.
ocular, systemic
 
 
Antivirals Aciclovir, topical or  Herpes simplex, zoster Inhibits herpes virus DNA synthesis  Ocular: blurred vision,
systemic 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 anaesthesia Topical or peri-ocular  Clinical exam Block conduction along the nerve fibres  Ocular: Irritation, corneal
injection. toxicicty.
Oxyburprocaine,  Systemic: generally
proxymetacaine. accidental intravascular or
Tetracaine, 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 toxin Injection at site of action  Motility disorder Prevents release of the neuro-  Dependant on treatment
transmitter acetycholine at sitee.e.g unwanted ptosis or
neuromuscular junctions double vision
Migraine
Pizotifen Serotonin Antagonist  Migraine 
5HT
Sumatriptan Acute Serotonin Antagonist  Migraine 
Migraine 5HT
Methysergide Long Serotonin Antagonist  Migraine 
term migraine 5HT

Urinary Tract Infection E.coli, proteus,  


saprophiticus.
Trimethoprim  UTI  NOT used in pregnancy
 Use nitrofurentoin instead
or amoxicillin
Amoxicillin  UTI  Used in pregnancy

Diazoxide  Insulinoma Blocks insulin release 


Teriparatide  Hypocalaemia PTH analogue 
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 action-
Cortisol 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 keeping blood sugars level.
Anti Inflammtory Effects and Immunosuppresive effects. Cotricosteroids have profound anti-inflamm effects. They suppress all phases of inflammatory response, include the early
swelling , redness pain and the later proliferative changes seen in chronic inflammtation. Inflammation is suppressed by several mechanisms
Circulating immunocompetent cells and macrophages are reduced and the formation of pro inflammatory mediators, as prostaglandins leukatrienes and platelet activating factor is
inhibited. Done by stimulating the synthesis in leucocytes of a protein (lipocortin) that inhibits phospholipase A2. This enzyme in cell membrane is activated in damaged cells adn
is responsible for the formation of arachdonic acid. The precursor of many inflammatory mediators. Corticosteroids suppress the genes coding for phospholipase A2, (COX2) and
the interleukin-2 (IL-2) receptor. These genes are normally switched on by NFkB but steroids induce the synthesis of IkB that binds to the NFkB and inhibits it by preventing its
entry into the nucleus. They also depress monocytemacrophages fintion and decrease T-Cells, IL1 and IL2 is inhibited.
Hydrocortisone Coritcosteroid  Anti Inflamm (iI)s used orally for replacement (ii) intra  Moon face, fat to trunk and
venously in shock and status face, purple striae,
asthmaticus and (iii) topically (e.g. hirsutism,acne, infections
ointments in eczema enemas in  Osteoporosis, bruise skin,
ulcerative colitis diabetes, hypercalaemia,
 Fluid retention,
hypokalaemia.
Prednisolone Corticosteroid  Anti Inflamm Is the most widely used drug driven  A s above
orally in inflammatory and allergic
diseases.
Betamethasone and Corticosteroid  Anti Imflamm Are very potent and have so salt-  As above
Dexamethasone retaining actions. This makes them
especially useful for high dose therapy in
conditions, such as cerebral oedema
where water retention would be a
disadvantage.
Beclometasone and Corticosteroid  Anti Inflamm Pass membranes poorly and are more  As above
Budesonide active topically than when given orally.
They are used in asthma and topically in
sever eczema to provide a local anti
inflammatory action with minimal
systemic effects.
Triamcinolone Corticosteroid  Anti Inflamm Used in sever asthma and by intra  As above
articular injection for local inflammation
of the joints.

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
 
 

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