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ACE inhibitors Ramipril, • Hypertension Block ATIATII by binding to • Hypotension

Lisinopril • Heart Failure the site on the enzyme that • Dry cough
• Post MI normally accommodates the (increased
terminal leucine of ATI. bradykinin)
Inhibits vasoconstriction. • Renal failure in pts
with bilateral renal
Beta-Blockers Atenolol, • Hypertension block β -adrenergic receptors inhibiting
• Provocation of
Propanolol • Angina the asthma, heart
• Arrhythmias effects of adrenaline and nonadrenaline.failure.
• Stable heart failure β 1 (heart) blockage decreases HR• Cold hands
and • Bradycardia -
contractility, β 2 (bronchial and fatigue
smooth muscle) blockage causes

Calcium Dihydropines – • Hypertension Vasodilation • Flushing, headache,

Channel Amlodipine, • Angina block cellular entry of Ca+ by • P.oedema
Blockers Phenyalkylamin • Supraventricular preventing opening of • Phenyalkylamines –
es - arrhythmia – voltage-gated L-type and T- can worsen heart
Verapamil, (Phenylalkylamines type calcium channels failure
Benzthiazepine only) • Gynaecomastia
s- • Impotence
Thiazide Bendrofluazide, • Hypertension increase water excretion by • Hypokalaemia
Diuretics hydrochlorothiazi • Combined with loop decreasing reabsorption of • Hyponatraemia
de for Heart Failure Na+ and Cl- in the distal • Hypotension
tubule by binding to the Cl- • Gout
site of the electroneutral • Type II DM
Na+/Cl- co-transport system
and inhibiting its action
causing a decrease in blood
volume, venous return and
Loop Diuretics Frusemide, • Hypertension (but Block Na+ resorption in • Hypokalaemia
Bumetanide less effective than ascending loop of Henle – • Hyponatraemia
thiazides – used diuretic effect. • Hypotension
when renal • Gout
impairment or
resistant to multiple
drug Tx)
• Heart Failure
Potassium- Spironolactone, • Secondary Blocks action of aldosterone • Hypokalaemia
sparing Amiloride Hypertension in distal convoluted tubule – • Hyponatraemia
diuretics • Severe heart Failure diuretic effect • Abdominal
Angiotensin II Losarten, • Hypertension Vasodilation – by inhibition • Usually mild
receptor Valsarten • Alternative to ACE at the angiotensin II receptor • No cough like in
antagonists inhibitor in heart ACE inhibitors
Alpha- Doxazosin, • Hypertension (in Reduces peripheral • Postural
adrenorecepto Prazosin addition to other resistance by inhibiting α 1- Hypotension
r antagonists hypertensives) adrenoreceptor-mediated • Dizziness
Fibrinolytics Streptokinase • Thrombolysis – Forms a complex with, and • Nausea/vomiting
Acute MI, stroke, PE activates, plasminogen into • Bleeding
Antiplatelet agents
Asprin • Prevention and Irreversibly inhibits COX and • Haemorrhage
treatment of MI and so stops synthesis of
stroke. Thromboxane A2 from
Arachidonic Acid which leads
to ↓ platelet aggregation.
Clopidogrel • Prevention and Inhibits activation of the • Haemorrhage
treatment of MI and glycoprotein IIb/IIIa receptor
stroke. on the surface of platelets
which is required for
aggregation to occur.
Warfarin • Prophylaxis+treatme Blocks reduction of Vit. K • Haemorrhage
nt DVT, PE epoxide → necessary for
Prophylaxis of synthesis of factors II, VII, IX
embolization in AF, and X.
Rheumatic disease +
prosthetic valves.

Heparin • Treatment of DVT, Activates antithrombin III, • Haemorrhage

PE. Prophylaxis of which limits blood clotting by
DVT/PE post op. inactivating thrombin and
• MI. factor X.
Statins Atorvastatin, • Prevention of Reversibly inhibit enzyme • Myopathy (muscle
Simvastatin, cardiovascular HMG CoA reductase which ache)
Pravastatin disease catalyses the rate-limiting • Disturbed LFTs
step in the synthesis of • Abdominal pain
HMG CoA→mevalonic
This ↓ in synthesis ↑ LDL
receptors so ↓ LDL levels.
Nitrates Glyceral trinitrate • Prophylaxis and Prodrugs – they decompose • Postural
(GTN), Isosorbide Treatment of angina. to form NO which activates hypotension
mononitrate • LVF guanylyl cyclase, thereby ↑ • Tachycardia
cyclic guanosine • Headache
monophosphate (cGMP). • Flushing
Protein kinase G is activated • Dizziness
and contractile proteins are
phosphorylated. This all
leads to Dilation of vessels.
Potassium Nicorandil (only • Prophylaxis of Relaxation of smooth muscle • Headache
channel licensed one) angina and vasodilation.
activators 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
Class Ia Quinidine, • VT Block Na2+ channels which • GI disturbances
Disopyramide, • WPW increases refractory period • Hypotension
Procainamide and in addition there is a
blockade of K+ channels
which delays repolarisation.
Class Ib Lignocaine, • Ventricular arrythmi, Block Na2+ channels but little • Nausea and
Mexiletine, especially VT effect on refractory period as Vomiting
Phenytoin K+ channels not blocked. ↓ • CNS toxicity
duration of the action • Hypotension
potential. • Bradycardia
Class Ic Flecainide • Pre-excitation AF Marked Na2+ channel • CNS toxicity
• cardioversion of blockage ↑refractory period, • Hypotension
paroxsms,AVNRT no effect on the duration of • Proarrythmogenic
,AVRT, WPW, AF , the action potential. after recent MI –
AT , NSVT (non- may increase
sustained VT) mortality

Class II Beta blockers • Junctional ↓ rate of spontaneous • Provocation of

(see above also) tachyarrhythmias, depolarisation of SA and AV asthma, heart
Paroxysmal nodal tissue failure.
events,AF, Flutter, ↓ conduction through AV • Cold hands
NSVT, SVT’s. node

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,

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
• 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
• GI disturbances
• Neurological
• 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
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.
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
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
Onset 20-30 minutes Peak
action 1-2 hrs Duration 3-4
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
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
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
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).

Ultralente Humulin UL A suspension of poorly • Hypoglycaemia

Ultratard 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)
Insulin Lantus Is soluble at acid pH. It has a • Hyoglycaemia
glargine long 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 • Lactic acidosis rare
Only diabetic • PCOS action of metformin is and limited to those
drug that reduces • Non Alcoholic fatty uncertain. It appears to act with impaired liver
cardiovascular liver disease mainly by reducing hepatic of kidney function.
risks. gluconeogenesis, it also • GI upset diarrhoea,
It reduces weight. decreases absorption of vomiting cramps.
glucose from the
gastrointestinal tract and
increases 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 • 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.

a- Glucosidase Acarbose • Type II diabetes Inhibits intestinal a- • Flautlence

inhibitors glycosidases, delaying the • Diarrhoea
digestion of starch and • Abdominal Pain
sucrose. It is taken with
meals and lowers the post
prandial increase of blood
Prolactinomas- oligomenorrhoea, amenoffhoea, galactorrhea, infertility, loss of libido, erectile dysfunction, osteoporosis. TRH
stimulates prolactin, Dopamine inhibits it.
Dopamine Bromocriptine • Prolactinoma Stimulates dopamine • Nausea
agonist drugs (ergot derivative) • Acromegaly receptors in the brain. • Psyhchiatric
Cabergoline • Hypogandism Symptoms
• Galactorrhea • Postural
• Fibrotic changes
which can lead to
valvular heart
Acromegaly Over secretion of GH =gigantism before puberty, acromegaly after puberty. (growth of hands feet, tightening of
Somatostatin Somatuline • Acromegaly Somatostatin analogue. • Gallstones
analogues Autogel Inhibits the production of GH. • Conratindicated in
Sandostatin LAR liver and kidney
Ocreotide failure, diabetes
Diabetes Insipidus (no ADH produced so leads to excretion of large volumes of isotonic water)
ADH analogue Desmopressin • Diabetes Insipidus Desmopressin is preferred to • Water retention
(nasal spray, vasopressin because it is a • Hyponatremia
tablets, or longer acting analogue. Make • Contraindicated in
subcutaneous sure to reduce fluid intake. heart failure, people
injection) using diuretics for
other conditions.
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
Thyroxine Levothyroxine • Hypothyroidism Administered orally is the • Concomitant
treatment of choice. conditions
Synthetic T4 is the sodium worsened by
salt of levothyroxine (L- thyroxine therapy.
thryoxine). Its effects are Heart disease, heart
delayed until the plasma failure, infarction,
protein and tissue binding angina, chronic lung
sites are occupied. disease,
Treatment is assessed by breathlessness,
monitoring TSH levels, which adrenal disease.
fall to normal when optimum Due to increase in
dose is achieved. Daily dose oxygen demand of
100 and 150ug best take on most tissues as well
waking. as myocardium
Liothyronine • Hypothyrioidism Is the sodium salt of T3 and • See above
because it 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
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 • Rashes
methimazole in vivo • Agranulocytosis
Once daily doses, 40mg for 1 • Patients should
month, then 30mg for 1 report a sore
month, 20mg for 1 month throat!
and then 10 mg daily until
reassessed.. Onset of action
3-4 weeks
Thionamides • Hyperthyroidism Possess a thiocarbamide • ?
group that is essential for immunosuppressive
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 • ?immunosupressive
intolerant of carbimazole.
Also inhibits the peripheral
deiodination of t4
Iodides • Hyperthyroidism Have poorly understood • Skin rashes
actions on the thyroid. They • Nausea
inhibit organification and and • Vomiting
hormone release. In addition • Allergic reaction.
iodide decreases the size
and vascularity of the
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. • Moon face
If acutely sick! • Striae
Take blood cortisol glucose • Fat redistribution
urea and electrolytes. Give • Hirsutsim
hydrocortisone 100mg as IV • Infection
bolus. Give saline infusion
• Proximal muscle
litre initially over 4-6 hours.
Correct hypoglycaemia iwth
IV bolus of 20% glucose. • Bruising
Continue with with IM
hydrocortisone 100mg 6
Long term
Hydrocortisone orally
10mg on waking, 5mg at
lunch and evening (dose
Fludrocortisone 0.1-0.2mg
per day.
Synthetic Fludrocortisone • Addisons Synthetic mineralcorticoid • Hypertension
Aldosterone derivative of aldosterone. • Oedema
Plasme rennin acitivity • Peptic ulcers
should be measured 2 hours • Mood changes
after the flurdrocortisone • GI upset
dose and maintained in the
• Glaucoma
normal range.
Cushings Syndrome Excess production of cortisol
Ketoconazole • Cushings Well absorbed orally, wide • Hepatic necrosis
• Anti fungal spectrum anti fungal drug • Adrenal suppression
which has adrenal
suppression effects
Metirapone • Cushings Metyrapone blocks cortisol • Nausea vomiting,
synthesis by inhibiting abdominal
steroid 11β-hydroxylase. cramping pain.
Mitotane • Cushings Unknown mechanism of • Dizzyness,
• Adrenal adenoma action but inhibits adrenal drowsyness nausea
steroidal action and vomiting.
Hyperparathyroidism and Malignancy account for 90% of Hypercalcaemia
Rehydration IV Saline • Hypercalcaemia Hydration must be • Hypernaetremia
maintained with IV
intravenous saline. This
will prevent severe
hypercalcaemia. Once
volume status is normal use
Bisphosphona Alendronate • Hypercalcaemia Bind to hyrdoxyapatite • GI upset, Erosion of
tes Etidronate crystals and reduce bone Oesophagus
Hypocalaemia Commonest cause is Vit D deficiency
Calcium Calcica • Hypocalaemia • Hypercalcaemia
Supplements Osteocare • Stomach pain
• Diarrhoea
Vitamin D Ergocalciferol Vit • Hypocalcaemia Vitamin D analogues allow • Hypercalcaemia
analogue D2 • Vit D deficiency absorption of calcium from
Cholecalciferol Vit the gut.
Alfacalcidol 1-
hydroxyvitamin D
Calcitriol 1,25
Dihydroxy D
Recombinant Teriparatide • Hypocalcaemia Stimulates bones resorption, • Dizzyness
PTH analogue • Hypoparathyriodism Kindey to re absorb calcium, • Leg Cramps
stimulates production of 1.25 • Nausea
Dehydroxyvit D at kidney.
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- Phenoxybenzami • Tumours of adrenal An irreversible antagonist is • Reflex tachycardia
adrenorecepto ne medulla used to block the a-effects of
r antagonist Labetalol the large amounts of
Doxazosin catecholamines from
Phentolamine tumours of the adrenal
Prazosin medulla.
b-blockers Atenolol (see • •
Conns excess production of aldesterone
Aldosterone Spironolactone • Conns Blocks the binding of • Severe
receptor (see above) • Liver disease with aldosterone to its receptor Hyperkaleamia
blockers Eplernone ascites and increases the excretion • Painful
of Na+ and decreases the Gyanocamastia
electrically coupled K+
Postassium Amiloride • Potassium sparing Decrease the luminal • Severe
Sparing Triamterene diuretic membrane Na+ permeability Hyperkalaemia
Diuretic • Conns 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 Common drugs • •
Kinetics Phenytoin,
Aspirin, Ethanol,
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
reactions cause
sever or fatal
hepatic failiure.
Focal Epilepsy Carbamazepine • Phenytoins anticonvulsant • Carbamazepine is
Phenytoin action is probably a result of metabolised in the
its ability to prevent high liver to
frequency repetitive activity. carbamzepine-
Phenytoin binds prerentially 10,11- epoxide, an
to inactivated (closed) Na+ active metabolite
channels stabilizing them in that partly
the inactivated state and contributes to both
preventing them from its anti-convulsant
returning to the resting action and
closed state which they must neurotoxicity. In
do before they can open contrast to
again. High freuquency phenytion there is a
repetitive depolarisation linear increase in
increases the proportion of serum
Na+ channels in the concentration with
inactivated state and, dosage. Mild
because these are neurotoxic effects
susceptible to blockade by are common
phenytoin, the Na+ is (nausea dizziness
progressively reduced until it drowsyness, blurred
is eventually insufficient to vision and ataxia)
evoke and action potential. Agranulocytosis is a
Neruonal transmission at rarer idyiosyncratic
normal frequencies is reaction.
relatively unaffected by • Phenytoin is
phenytoin because a smaller hyroxylated in the
portion of the Na+ channels liver by a saturable
are in the inactivated state. enzyme system.
Carbamazepine, lamotrigine, The rate of
valproate, and topiramate. metabolism varies
Have similar actions on greatly in patients.
neuronal Na+ channels. 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
disturbance occur
(nystagmus, ataxia,
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
Absence Ethosuximide • Absence seizures involve • Ethosuximide-
Epilepsy in Sodium Valproate oscillatory neuronal activity Nausea vomiting.
Children between the thalamus 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
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
Levodopa Sinemat • Parkinsons Levodopa is the immediate • Nausea and
Madopar precursos of dopamine and is vomiting caused by
Both these drugs able to penetrate the brain stimulation of the
come with where it is converted to CTZ.
extracerebral dopamine. The site of the • Psych effects vivid
decarboxylase decarboyxlation is uncertain, dreams,
inhibitors) but as dopa decarboxylase is hallucinations,
no rate limiting there maybe psychotic states
sufficient enzyme in the and confusion.
remaining dopaminergic • Postural
nerve terminals. Another hypotension is
possibility is that the common.
conversion occurs in nor • Dyskinesias (jerky
adrenergic or seratonergic
terminals. Because the de- or dance like
carboxylase activity in these movement) are an
neurones is not specific. important adverse
• Long term after five
years treatment
about 50% of
patients will have
lost ground. In some
there is a gradual
recurrence of
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
Dopamine Bromocriptine • Parkinsons Dopamine agonists have no • Nausea, psychiatric
Receptor (ergot derivative) • Prolactinomas advantage over levopdopa symptoms, postural
Agonists Ropinirole (non and the adverse effects are hypotension.
ergot derivative) similar. • Pulmonary fibrosis
Apomorphine Used with young patients, in and retroperitoneal
(very powerful particular who are given a fibrosis.
given by dopamine agonist as initial • Apomorphine
parenteral therapy (sometimes together (highly emetogenic)
administration) with selegeline). This domperidone should
strategy may slow the be given before
development of dyskinesias treatment started.
but only 50% of patients
show any beneficial 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
Pre Synaptic Amantadine • Parkinsons Potentiates dopamine by • Dizzyness, Loss of
Re-Uptake preventing re-uptake in the co-ordindation,
inhibitor pre-synaptic terminals. inability to sleep,
Moderate effect but toleranc nausea,
soon develops nervousness
Monamine Selegiline • Parkinsons Inhibits monoamine oxidase • Nausea
oxidase type B (MAO-B) there by • Heartburn
inhibitor type increasing dopamine. This is • Dry mouth
B (MAO-B) 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
COMT Entacapone • Parkinsons Inhibbits catechol-O- • 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
Antimuscarini Benzetropine • Parkinsons Produce a modest • Dry mouth
cs Procyclidine iimprovement in the early • Urinary retention
Orphenadrine stages of parkison’s 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 • Myaesthenia gravis Most widely used drug; it has • 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 • MND Used to treat amyoptrophic • 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) • Guillen Barres Either high-dose intravenous • Hepatitis
immunoglobul immunoglobulins (IVIg) at • Renal failure
ins 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, • Glaucoma Reduce aqueous secretion by • Ocular irritation
betaxolol, inhibitory action on beta • Bronchospasm
levobunolol adrenoreceptors in the • Bradycardia
cilliary body. • Nightmares
• Exacerbation of
hear failure
Muscarinic Pilocarpine (also • Glaucoma Increase aqueous outflow via • 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
Alpha2- Brimonidine, • Glaucoma Reduces aqueos secretion by • 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 • Glaucoma Reduce aqueous secretion by • Ocular route:
Anhydrase (systemic) the cilliary body irritation and allergy
Inhibitors Dorzolamide, • Systemic route:
Brinzolamide Malaise,
paraesthesia, urea
and electrolye
aplastic anaemia
Mydriatics and cycloplegics – ( Used for retinal examination and objective refraction (retinoscopy)
Antimuscarini Tropicanamide, • Eye dilation for exam Inhibit muscarinic receptors • Ocular: Blurred
cs cyclopentolate, of parasympathetic nervous vision, glare, angle
atropine. system to paralyse papillary closure glaucoma.
sphincter and ciliary muscle. • Systemic:
Tachycardia, dry
mouth, confusion,
Alpha- Phenylephrine • Eye dilation for exam Stimulates dilator muscle of • Ocular: Blurred
stimulant the pupil no cycloplegic vision, glare, angle
effect. closure, glaucoma,
• Systemic
Lubricants – There are a wide range
Carbomers, • Dry eye Exact mechanism depends • Ocular: Allergy,
hyrpmellose, on the agent blurred vision
polyvinyl alcohol,
liquid paraffin
Ant-Inflammatory Agents. Most important drugs are corticosteroids, a Variety of other drugs are available including systemic
Corticosteroid Prednisolone, • Suppress Suppresion of broad • Ocular: Glaucoma
s betamethasone, Inflammation spectrum of inflammatory (especially with
dexamethasone processes (see local
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
Mast cell Cromoglicate, • Allergy Stabilise mast cells • Occular: Irritation
stabilisers nedocromil,
Anti- Topical: • Allergy Block histamine receptor • Occular route:
histamines Antazoline, Irritation
azelastine, • Sytemic route:
levocabastine. Drowsiness
NSAIDS Topical: • Eye inflammation Modulate prostaglandin • Systemic: Peptic
(ketorolac, production. ulceration, 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 • Vary with agent
Chloramphenicol, specificities • Ocular: allergy;
gentamicin, corneal toxicity
ciprofloxacin, common with
Neomycin, fusidic intensive use.
acid. • Systemic: generally
Occassionally only with systemic
intra-ocular, use.
• •
• •
Antivirals Aciclovir, topical • Herpes simplex, Inhibits herpes virus DNA • Ocular: blurred
or systemic zoster synthesis vision, corneal
• Systemic: Rashes:
kidney, liver and
other effects may
occur with systemic
Local Anaesthetics: Major uses are to relieve pain and thereby assist with clinical examination and the facilitation of surgical
Local Topical or peri- • Clinical exam Block conduction along the • Ocular: Irritation,
anaesthesia ocular injection. nerve fibres corneal toxicicty.
Oxyburprocaine, • Systemic: generally
proxymetacaine. accidental
Tetracaine, intravascular or
lidocaine. intrathecal
(cerebrospinal fluid)
injection. During
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 • Motility disorder Prevents release of the • Dependant on
toxin action neuro-transmitter treatment sitee.e.g
acetycholine at unwanted ptosis or
neuromuscular junctions double vision
Pizotifen Serotonin • Migraine •
Sumatriptan Serotonin • Migraine •
Acute Antagonist
Migraine 5HT
Methysergide Serotonin • Migraine •
Long term Antagonist
migraine 5HT

Urinary Tract E.coli, proteus, • •

Infection saprophiticus.
Trimethoprim • UTI • NOT used in
• Use nitrofurentoin
instead or
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.
Hydrocortison Coritcosteroid • Anti Inflamm (iI)s used orally for • Moon face, fat to
e replacement (ii) intra trunk and face,
venously in shock and status purple striae,
asthmaticus and (iii) topically hirsutism,acne,
(e.g. ointments in eczema infections
enemas in ulcerative colitis • Osteoporosis, bruise
skin, diabetes,
• Fluid retention,
Prednisolone Corticosteroid • Anti Inflamm Is the most widely used drug • A s above
driven orally in inflammatory
and allergic diseases.
Betamethason Corticosteroid • Anti Imflamm Are very potent and have so • As above
e and salt-retaining actions. This
Dexamethaso makes them especially
ne useful for high dose therapy
in conditions, such as
cerebral oedema where
water retention would be a
Beclometason Corticosteroid • Anti Inflamm Pass membranes poorly and • As above
e and are more active topically
Budesonide 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 • As above
intra articular injection for
local inflammation of the

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
• •
• •