solve questions of pharmacology

1. WRITE DOWN THE RATIONAL OF
FOLLOWINGS:
1. Aspirin in post myocardial infarction.
ANS: By inhibiting the platelet aggregation aspirin lowers the incidence of
reinfarction. TXA2 synthesis in platelet is inhibited in low doses. Aspirin
reduces the transient ischaemic attack and lowers the incidence of stroke in
such patients. But the risk of stroke in postMI patients is not reduced.
Dose: 60-100 mg/day
But it has been argued that high dosecan reverse the beneficial effects
concurrently inhibiting PGI2 synthesis in vessel wall.
2. Disulfuram in alcoholism:
ANS: Disulfuram has been used as an aversion technique in chronic
alcoholics who are motivated and sincerely desire to leave the habbit. It
inhibits the enzyme aldehyde dehydrogenase probably after conversion into
active metabolites. When alcohol is ingested after taking disulfuram, the
concentration of acetaldehyde in tissue and blood rises and a number of
highly distressing symptoms (aldehyde syndrome) are produced promptly.
Due to which the personstops the drinking.
3. Folic acid in pregnancy:
ANS: Folic acid is used in the pregnancy due to the increased demand to
meet the metabolic functions of the bodyand prevents the anaemia in
pregnancy. Folic acid is vital to supportthe healthy development of a baby’s
brain and spinal cord. Before you are even aware that you’re pregnant, your
baby’s brain and spinal cord are already forming. By having enough folic
acid in your blood at this important time you help to ensure that they
develop properly. Many women don't realise that taking folic acid can help
to avoid the possibility of some very serious consequences.

2. 4. Naloxone usedfor morphine poisoning:
ANS: Naloxone is the drug of choice for morphine poisoning. It is N-
alylnor-oxymorphine and a competitive antagonist on all type of opioid
receptors. However, it blocks µ- receptors at much lower dosethan those
needed to block kappa and delta receptors. So, it blocks the effects of
morphine completely.
5. Acetazolamide in mountain sickness:
ANS: Acute altitude sickness usually occurs during the first few days at
altitude, before respiratory acclimatization is complete. Thus at high
altitudes, climbers hyperventilate in responseto lower oxygen levels. This
results in reduced carbon dioxide(an acid) and reduced oxygen level in the
body.
Herein, lies the rational for prophylaxis with acetazolamide inhibits renal
carbonic anhydrase causing bicarbonate dieresis and extracellular acidosis.
Acetazolamide has, however been shown repeatedly to lower blood pH,
improve blood gas, and improve symptoms scores for acute mountain
sickness.
In nephron, CO2 is lipophilic and rapidly diffuse across the luminal
membrane into the epithelial cell, where it reacts with water to form
bicarbonate, a reaction catalyzed by cytoplasmic carbonic anhydrase.
Acetazolamide increases CO2 levels in peripheral tissues and decrease CO2
levels in expired gas.
It is usefull in treating established acute mountain sickness. Doses used have
varied from 250mg to 1 gm, and probably 500mg daily as a sustained release
preparation begun in nthe 24 hours before ascent is adequate.

3. 6. Sublingual nitroglycerine tablets:
ANS: When nitroglycerine is administered orally, most of each doseis
destroyed on its first pass through liver. The sublingual route is used when
terminating an attack or aborting an imminent one is the aim. The tablet may
be crushed under the teeth and spread over the buccal mucosa. It acts
within 1-2 min becauseof direct absorptioninto the systemic circulation
bypassing the liver where 90% is metabolized.
7. Sodium intake is restrictedin hypertension:
ANS: salt is essential to our bodies. Normally the kidneys control the level
of salt. If there is too much salt, the kidneys pass it into urine. But when our
salt intake levels are very high, the kidneys can not keep up and the salt ends
up in our bloodstream. Salt attracts water. When there is too much salt in
the blood, the salt draws more water into the blood. More water increases the
volume of blood which raises blood pressure.
Almost 80% of the average person’s daily salt intake comes from processed
foods. If we ate only natural foods and limited the use of table salt, we
would be able to eliminate excess salt in our body.
A lower sodium diet is good for people who are older, who are of
African American descent, or who have high blood pressure or diabetes.
These folks should limit their sodium intake to no more than 2300-2400mg a
day.people with heart failure or kidney disease are advised to keep their
sodium intake under 2000mg per day.

4. 8. Atropine is given in organophosphorus poisoning:
ANS: Atropine is the specific antidote for anticholinesterase
( organophosphate)so, it is highly effective in counteracting the muscarinic
symptoms, in higher doses it also antagonize the central effects. It does not
reverse the peripheral muscular paralysis which is a nicotinic action. In all
cases of anti-ChE (carbamate or organophosphate) poisoning must be
promptly given atropine 2mg i.v. repeated every 10 min till dryness of
mouth or other signs of atropinization appear. Continued treatment with
maintainance dosemay be required for 1-2 weeks.
9. Salicylates are not given in empty stomach:
ANS: The most important adverse effect of salicylate is gastric mucosal
damage and peptic ulceration especially when given in empty stomach. This
is due to the inhibition of COX-1 mediated synthesis of gastroprotective
prostaglandins i.e. PGE2, PGI2.deficiency of PGEs reduces mucus and
HCO₃⁻ secretion tends to enhance acid secretion and may promotemucosal
ischaemia leading to peptic ulceration and the chance of inhibition of PGs
synthesis is more when given in empty stomach. So, these drugs are not used
in empty stomach.
WRITE DOWN THE RATIONAL OF:
10.Carbidopa and le vodopa combination:
ANS: Levodopa undergoes high first pass metabolism in gastrointestinal
mucosa and liver. About 1% of administered levodopa that enters brain
when used alone.
Carbidopa is an extracerebral dopadecarboxylase inhibitors; they do not
penetrate the blood-brain barrier and do not inhibit conversion of levodopa
to dopamine in the brain. Administered along with levodopa, they increase
its half-life in the periphery and make more of it available to cross blood-
brain barrier to reach its site of action.

5. The benefits of the combination are:
i. The plasma half-life of levodopa is prolonged and its doseis
reduced to approximately 1/4th.
ii. Systemic concentration of dopamine is reduced, nausea and
vomiting are not prominent, therapeutic doseof levodopa can be
attained quickly.
iii. Cardiac complications are minimized.
iv. Pyridoxine reversal of levodopa effects does not occur.
v. “on-off” effect is minimized since cerebral dopamine levels are
more sustained.
vi. Degree of improvement may be higher; some patients, not
responding adequately to levodopa alone, also improve.
Combination of levodopa with carbidopahas been given the name
“co-careldopa”.
11. Furosemide with amiloride:
ANS: furosemide is high efficacy loop diuretics and inhibits the Na⁺-k⁺-
2Cl⁻ cotransport in ascending limb of loop of hanle. Potassium excretion is
increased due to high sodium load reaching distal tubule.
Amiloride is non-seroidal organic bases which cause decrease potassium
excretion, particularly when it is high due to large K⁺ intake or use of
diuretic that enhances K⁺ loss i.e. furosemide. Unlike spironolactone their
action is independent of aldosterone.
They act on luminal membrane of distal tubule cells to inhibit elecrogenic
Na⁺ reabsorption.
Therefore, by giving these two drung in combination the level of K⁺ can be
maintained in the blood and the risk of hypokalemia is minimized.

6. 12.Nifidipine and beta-blockers:
ANS: Nefidipine is a calcium channel blocker which cause reflex
tachycardia, increased contractility and cardiac output.
Beta-blockers cause ventricular dilatation.
By giving combination of these two drugs, following advantages can be
achieved:
I. Reflex tachycardia due to CCBs is blocked by beta-blockers.
II. The tendency of beta-blockers to cause ventricular dilatation is
counteracted by CCBs.
III. The tende3ncy of beta-blockers to reduce total coronary flow is
opposedbyCCBs.
13. Thiazide and spironolactone:
ANS: Thiazidse diuretics cause hypokalemia by increasing the loss of
potassium leading to weakness, fatigue, muscle cramps, cardiac arrhythmias.
Decrease plasma potassium level also inhibits the release of insulin leading
to hyperglycemia.
Spironolactone is a aldosterone antagonist. It blocks the receptor on
which aldosterone acts. This leads to inhibition of reabsorption of sodium
and inhibition of secretion of potassium in the late part of distal tubule
resulting in i9ncreased excretion of sodium and retention of potassium in the
body.
So, by giving these two drugs in combination, the level of potassium can
be maintained in the bodyand the risk of hypokalemiaa is minimized.

7. 14. Classifyantipsychotic and antiepileptic. Explain pharmacological action
and use of chlorpropamide and carbamazepine:
ANS: Psychoses are the severe psychiatric illness with serious distortion of
thought, behavior, capacity to recognize reality and of perception (delusions
and hallucinations). There is in explicable misperception and misevaluation;
the patient is unable to meet the ordinary demands of life.
Anti-psychotic drugs are the agents having primary effects on psyche
(mental process)and are used for treatment of psychiatric disorders.
CLASSSIFICATIONOF ANTI-PSYCHOTIC DRUGS:
I. Phenothiazines:
 Chlorpromazine
 Triflupromazine
 Trifluperazine
II. Butyurophenones:
 Haloperidol
 Trifluperidol
 Penfluperidol
III. Thioxanthenes:
 Flupenthixol
IV. Other heterocyclics:
 Pimozide
 Loxapine

8. V. Atypical antipsychotics:
 Clozapine
 Risperidone
 Olanzapine
 Ziprasidone
Pharmacological actions of chlorpromazine:
a) CNS: effects differ in normal and psychotic individuals:
In normal individuals chlorpromazine produces indifference to
surroundings, paucity of thought, psychomotorslowing, emotional
quietening, reduction in initiative and tendency to go off to sleep from which
the subject is easily arousable. Spontaneous movements are minimized butr
slurring of speech, ataxia or motor incoordination does not occur.
In a psychotic individual, chlorpromazine reduces irrational behavior,
agitation and aggressiveness and controls psychotic symptomology.
Disturbed thought and behavior are gradually normalized, anxiety is
relieved. Hyperactivity, hallucination and delusions are suppressed.
b) ANS: chlorpromazine have varying degree of alpha adrenergic blocking
activity. It also have a weak H₁-antihistamine and anti-5HT actions as well.
c) Local anaesthetics: chlorpromazine is as potent a local anaesthetic as
procaine. However, it is not used for this purposebecause of its irritant
action.
d) CVS: high doseof chlorpromazine directly depress the heart and produce
EEG changes. Chlorpromazine exerts some antiarrhythmic action, probably
due to membrane stabilization. Arrhythmia may occurin overdose.

9. e) Skeletal muscle: neuroleptics have no effect on muscle fibres or
neuromuscular transmission. They reduce certain types of spasticity; the site
of action being in the basal ganglia or medulla oblongata. Spinal reflexes are
not affected.
f) Endocrine: neuroleptics consistently increase prolactin release by blocking
the inhibitory action of dopamine on pituitary lactotropes. This may result in
galactorrhoea and gyaecomastia.
Uses of chlorpromazine:
i. Psychoses:
 Schizophrenia
 Mania
 Organic brain syndromes
ii. Anxiety
iii. As anti-emetics
iv. Other uses:
 To potentiate hypnotics, analgesics and anaesthetics.
 Tetanus, CPZ is secondarydrug to achieve muscle relaxation.
 Alcoholic hallucinations.
CLASSIFICATIONOF ANTI-EPILEPTICS:
i. Barbiturates:
 Phenobarbitone
ii. Deoxybarbiturate:
 Primidone
iii. Hydantoin:

10.  Phenytoin
 Fosphenytoin
iv. Iminostilbene:
 Carbamazepine
 Oxcarbazepine
v. Succinimide:
 Ethosuximide
vi. Aliphatic carboxylic acid:
 Valproic acid
 Divalproex
vii. Benzodiazepines:
 Clonazepam
 Diazepam
 Lorazepam
 Clobazam
viii. Phenyltriazine:
 Lamotrigine
ix. Cyclic gaba analogue:
 Gabapentin
x. Newer drugs:
 Vigabatrin
 Topiramate
 Tiagabine
 Zonisamide
Uses of carbamazepine:
a) Complex partial seizures
b) General tonic clonic seizure
c) Simple partial seizure
d) Trigeminal and related neuralgias
e) Manic depressive illness and acute mania.

11. 15.Describe the pharmacotherapy of hypertension and gout:
ANS: the general principles of antihypertensive therapy enunciated in JNC7
and WHO-ISH guidelines is as follows:
a) Except for stage-2 hypertension, starts with a single most appropriate
drug which for majority of patients is thiazide. However, a beta-
blocker, ACE inhibitor or CCB may also be considered.
b) Initiate therapy at low dose;if needed increase dosemoderately.
Thiazide doseshould be 12.5-25mg/day hydrochlorthiazide or
equivalent.
c) Majority of stage-2 hypertension are started on a 2 drug combination;
one of which usually is a thiazide diuretic.
d) If only a partial response, add a drug from another complimentary class
or change to low dosecombination.
e) If no response, change to a drug from another class or low dose
combination from another classes.
f) In case of side effect to the initially choosendrug, either substitute with
drug of another class or reduce doseand add a drug from another class.
Drugs and their doses:
 Hydrochlorthiazide- 12.5 mg OD
 Furosemide-20-80mg/day
 Atenolol-25-50mg OD
 Amlodipine-2.5-5mg OD
 Lisinipril-2.5-5mg OD
 Losarton-25-50mg OD
Pharmacotherapy of gout:
For acute gout:
a. NSAIDs: one of the strong anti-inlammatory drugs, e.g. indomethacin,
naproxen, piroxicam, or etoricoxib is given in relatively high doseand
quickly repeated doses. Theyare quite effective in terminating the attack.

12. b. Colchicines is neither analgesic nor anti-inflammatory, but it especially
suppress gouty inflammation. It does not inhibit the synthesis or promote the
excretion of uric acid. Thus, it has no effect on blood uric acid levels.
c. Corticosteroids: intraarticular injection of a soluble steroid suppress the
symptoms of acute gout. Crystalline preparations should not be used. It is
indicated in refractory cases and those not tolerating NSAIDs/ colchicines.
E.g. prednisolone 40-60mg/day
For chronic gout:
a. Uricosuric drugs:
 Probenecid: uric acid is largely reabsorbed by active transport,
while less of it is secreted; only 1/10th of filtered load is
excreted in urine. Probenecid therefore, promotes its excretion
and reduces its blood level.
Dose 0.25-0.5mg BD
 Sulfinpyrazone: it is a pyrazolone derivative related to
phenylbutazone having consistent uricosuric action, but is
neither analgesic nor anti-inflammatory. At the usual
therapeutic doses, it inhibits tubular reabsorption of uric acid.
Dose: 100-200mg BD.
b. Uric acid synthesis inhibitors:
 Allopurinol: allopurinol is the first choice drug in chronic gout.
It can be used in both over producers and under excretors of
uric acid, particularly more serious case, with tophi or
nephropathy.
Dose start with 100mg OD , gradually increase to maintenance
doseof 300mg/day; maximum 600mg/day

13. 16.Describe vasomotorreversalofdale:
ANS: Rapid i.v. injection of adrenaline produces a marked increase in both
systoloic as well as diastolic blood pressure(at high concentration α-response
predominates and vasoconstriction occurs even in skeletal muscle). The blood
pressure returns to normal within a few minutes and a secondaryfall in mean
BP follows. The mechanism is rapid uptake and dissipation- concentration of
adrenaline decreases, This adrenaline concentration cannot stimulate alpha
receptors but is enough to stimulate Beta receptors. Hence there is a secondary
fall in blood pressure. So when rapid i.v. injection of adrenaline is given in
combination with Alpha blockers, only fall in BP is seen which is called
Vasomotor Reversal Of Dale.
17. Differentiatebetween:
A. Drug potency and drug efficacy:
Drug potency:
1) It is the relationship between the the doseof a drug and the therapeutic effect.
2) It refers to the drug's strength.
3) A drug is considered potent when a small amount of the drug achieves the
intended effect.
4) It depends on bothaffinity and efficacy of drug.
5) It is a factor in choosing the doseof drug.

14. Drug efficacy:
1) It is the ability of a drug to producethe desired therapeutic effect.
2) It refers to the drug's effectiveness.
3) A drug is considered efficacious when a drug achieves the maximal responses
that can be elicited by it.
4) It depends on bothdrug binding and drug bound receptor.
5) It is a decisive factor in choosing the drug.
B. Synergism and antagonism:
Antagonism
1) When one drug decreases or abolishes the action of another, they are said to be
antagonistic and the phenomena is called antagonism.
2) In an antagonistic pair one drug is inactive as such but decreases the effect of
other.
3) It can be represented as:
•Effects of drugs (A+B) <Effects of drug A+ Effects of drug B
4) Eg:
•Atropine - ACh
•Morphine - Naloxone
•Glucagon and insulin on blood sugar level.
Synergism:
1) When the action of one drug is facilitated or increased by the other, they are
said to be synergistic and the phenomena is called synergism.

15. 2) In a synergistic pair, both the drugs can have action in same direction or given
alone one may be inactive but still enhance the action of the other when given
together.
3) It can be represented as :
•Effects of drugs (A+B) =Effects of drug A+ Effects of drug B
•Effects of drugs (A+B) >Effects of drug A+ Effects of drug B
4) Eg :
•Aspirin + Paracetamol= as analgesic / anripyreti
•Ephedrine + Theophylline= as bronchodilator
•Amlodipine+ Atenolol = as antihypertensive
•Levodopa+ Carbidopa = Inhibition of peripheral metabolism
C. Tubocurarine and succinylcholine
Tubocurarine:
1) It belongs to non- depolarizing or competitive blockers.
2) It work by competitively blocking the binding of acetylcholine to its receptors.
3) They bind to acetlycholine receptors as antagonist and leaves fewer receptors
available for acetylcholine to bind.
Succinylcholine:
1) It belongs to depolarizing blockers.
2) It work by depolarizing the plasma membrane of muscle fibre.
3) They bind to acetylcholine receptorand cause depolarization by opening sodium
ion channels just like acetylcholine does.

16. D. Respiratoryalkalosis andrespiratory acidosis:
Respiratory alkalosis:
1) When the pH value of bodyfluids becomehigher than 7.45 due to
abnormalities in respiratory system then it is called respiratory alkalosis.
2) It is caused by hyperventilation of lungs.
3) In this, rate at which CO2 is eliminated from body fluids through the lungs
increases.
4) It may be produced accidentally during excessive mechanical ventilation. Other
causes include: psychiatric causes like anxiety , hysteria, stress ; CNS causes like
stroke, subarachnoid haemorrhage, meningitis ; drugs like doxapram , aspirin ,
caffeine; high altitude; lung disease such as pneumonia; pregnancy.
5) Kidneys help to compensate for respiratory alkalosis by decreasing the rate of
secretion of hydrogen ions into filtrate and reabsorption of bicarbonate ions.
Respiratory acidosis:
1) When the pH value of bodyfluids becomelower than 7.35 due to abnormalities
in respiratory system then it is called respiratory acidosis.
2) It is caused by hypoventilation of lungs.
3) In this, rate at which CO2 is eliminated from body fluids through the lungs
decreases.
4) Its causes include : CNS problems such as myasthenia gravis, muscular
dystropy; traumas ;airway obstruction related to asthma or chronic obstructive
pulmonary disease (COPD) exacerbation; hypoxia.
5) Kidneys help to compensate for respiratory acidosis by increasing the rate of
secretion of hydrogen ions into filtrate and reabsorption of bicarbonate ions.
18. Write down the adverse drug reactions of the following:
a) Amphetamine:

17. More common
 Bladder pain
 bloody or cloudy urine
 difficult, burning, or painful urination
 fast, pounding, or irregular heartbeat or pulse
 frequent urge to urinate
 lower back or side pain
 Anxiety
 dry mouth
 lack or loss of strength
 stomach pain
 weight loss
Less common
 Cold or flu-like symptoms
 cough or hoarseness
 fever or chills
b) Lignocaine:
More common
 Flushing, redness of the skin
 small red or purple spots on the skin
 swelling at the site of application
 unusually warm skin
Less common
 Bruising, burning, pain, or bleeding at the site of application
 itching skin

18. c) Warfarin:
 Abdominal or stomach pain with cramping
 bleeding gums
 blood in the urine
 bloody stools
 blurred vision
 burning, crawling, itching, numbness, prickling, "pins and needles", or tingling
feelings
 chest pain or discomfort
 confusion
 coughing up blood
 difficulty with breathing or swallowing
 dizziness, faintness, or lightheadedness when getting up suddenly from a lying
or sitting position
 excessive bruising
 headache
 increased menstrual flow or vaginal bleeding
 nosebleeds
 paralysis
 peeling of the skin
 prolonged bleeding from cuts
 red or black, tarry stools
 red or dark brown urine
 shortness of breath
 sweating
 unexplained swelling
 unusual tiredness or weakness

19.  red, sore, or itching skin
 sores, welting, or blisters
 unusual drowsiness, dullness, or feeling of sluggishness
d) Furosemide:
 Chest pain
 chills
 cough or hoarseness
 fever
 general feeling of tiredness or weakness
 headache
 lower back or side pain
 painful or difficult urination
 shortness of breath
 sore throat
 sores, ulcers, or white spots onthe lips or in the mouth
 swollen or painful glands
 tightness in the chest
 unusual bleeding or bruising
 unusual tiredness or weakness
 wheezing
e) Acetylcholine:
Hypotension
Bradycardia
Flushing, and sweating

20. Ocular side effects have rarely included corneal clouding, corneal decompensation,
and corneal edema
Bronchospasmin a patient on concomitantmetoprolol therapy.
f) Aspirin:
epigastric pain
Heartburn
Nausea and vomiting
Ulcers
Gastric mucosal lesions
Hemorrhage and peptic ulcers
Renal side effects include reduction in glomerular filtration rate (particularly in
patients who are sodium restricted or who exhibit diminished effective arterial
blood volume, suchas patients with advanced heart failure or cirrhosis), interstitial
nephritis, papillary necrosis, elevations in serum creatinine, elevations in blood
urea nitrogen, proteinuria, hematuria, and renal failure.
Hypersensitivity side include bronchospasm, rhinitis, conjunctivitis, urticaria,
angioedema, and anaphylaxis
Hepatotoxicity and cholestatic hepatitis
Central nervous system side effects include agitation, cerebral edema, coma,
confusion, dizziness, headache, cranial hemorrhage, lethargy and seizures
g) Morphine in CNS:
Respiratory depression

21. Apnea and to a lesser degree
Circulatory depression
Respiratory arrest
Shockand cardiac arrest
Constipation, nausea
Lightheadedness, dizziness
Sedation
Vomiting and sweating
Bradycardia, hypertension, hypotension, palpitations
Biliary pain, dyspepsia, dysphagia, gastroenteritis, abnormal liver function tests,
rectal disorder, thirst
Nervous System: abnormal dreams, abnormal gait, agitation, amnesia, anxiety,
ataxia, confusion, convulsions, coma, delirium, depression, dry mouth, euphoria,
hallucinations, lethargy, nervousness, abnormal thinking, tremor, vasodilation,
vertigo, headache.
h) Benzodiazepines:
Hypotension
Cardiac arrhythmias
Slow heart rate
Apnea
Respiratory depression
Nausea/vomiting
Blurred vision or double vision

22. 19. Write down the use of acetazolamide in glaucoma:
An increase in pressurewithin the eye can lead to damage to the optic nerve at the
back of the eye. When this occurs it is called glaucoma. Glaucoma can lead to a
loss of vision if it is not treated. Treatment with acetazolamide helps to reduce eye
pressure, and this helps to prevent further eye damage.
Acetazolamide works by blocking the action of an enzyme called carbonic
anhydrase. Blocking this enzyme reduces the amount of fluid in eye i.e. aqueous
humor and this helps to lower the pressure within the eye.
20. Write the drugs commonly used in the managemaent of myasthenia
gravis and describe their mechanism of action ?
Ans. -Mysthenia gravis is an autoimmune disorder affects 1 in 10000 populations
-characterized by the development of antibodies directed to the nicotinic receptors
at the muscle end plate and
-this results in the reduction of NM cholinoreceptors to 1/3rd of normal or less.
- structural damage to the neutomuscular junction results feel weakness and fatigue
on repeated activity with recovery after rest.
Commonly used drugs to treat this disorder can be listed as-
1) Anticholineesterase : Neostigmine(preferred 15 mg QID), Physostigmine etc
2) Corticosteroids: Prednisolone( 30-60mg od)
3) Other immunosuppresants( eg. Azathioprine, Cyclosporine,etc.)
Other mechanisms
4) Plasmapharesis( plasma exchange)
5) Thymectomy( removal of thymus gland)
Short mechanism of action of drugs
1) Anticholineesterase : Neostigmine(preferred), Physostigmine etc
Reversibly binds at the esteric site of cholinesterase enzyme

23. Prevents the hydrolysis of Ach
Increase the interaction between Ach-nicotinic receptor
2) Corticosteroids: Prednisolone
Inhibit the production of nicotinic receptor antibodies
Immunosuppresant action
May increase the synthesis of nicotinic receptors
3) Other immunosuppresants
Immunosuppresants inhibit the nicotinic receptor antibody by selectively
suppressing the cell mediated immunity.
21. Why acetazolamide is used in Glaucoma?
Ans: Acetazolamide is a carbonic acid anhydrase enzyme inhibitors.
Acetazolamide
( ─)
H2O + CO2 H2CO3 H+ + HCO3-
When acetazolamide (0.25 gm tablet 6-12 hourly) is administered orally, it reduces the
formation of aqueous humor by limiting the generation of bicarbonate in, because
carbonic acid is the main component of aqueous humor. Hence, along with other ocular
hypertensive drug, it reduces the intraocular pressure and thus used in the treatment of
open angle glaucoma.