Categories
Uncategorized

LEARN ABOUT ANTIPARKINSONIAN DRUGS

ANTIPARKINSONIAN DRUGS

Parkinson’s disease was first described by sir James Parkinson. It is characterised by tremor, rigidity, bradykinesia, and loss of postural reflexes.

In idiopathic parkinsonism there is degeneration of the dopamine-containing neurons in the substantia nigra, resulting in dopamine deficiency. Hence, the balance between inhibitory dopaminergic neurons and excitatory cholinergic neurons is disturbed resulting in relative cholinergic overreactivity.

Classification :

  1. Drugs influencing brain dopaminergic system

a. Dopamine precursor: levodopa

b. Dopamine agonists: bromocriptine, pergolide, pramipexole, ropinirole

c. Dopamine releasing drug: amantadine

d. MAO-B inhibitors: rasagiline

e. COMT inhibitors: tolcapone, entacapone

f. Peripheral decarboxylase inhibitors: carbidopa, benserazide

  1. Drugs influencing brain cholinergic system

a. Centrally acting anticholinergic drugs: benzhexol, procyclidine, benztropine

b. Antihistaminics with anticholinergic activity: promethazine, diphenyhydramine

The main aim of drug therapy in parkinsonism is to either enhance dopamine activity or reduce cholinergic activity in the striatum.

DOPAMINE PRECURSOR: LEVODOPA

Levodopa is the main drug for the treatment of idiopathic parkinsonism. Dopamine does not cross BBB hence its immediate precursor levodopa is used. It is converted to dopamine by decarboxylase enzyme. A large amount of the drug is converted to dopamine in the peripheral tissues by peripheral decarboxylase enzyme. Only a small amount of levodopa enters the brain. Therefore levodopa is always used in combination with carbidopa /benserazide(peripheral decarboxylase inhibitors) which does not cross the BBB. ; peripheral metabolism of levodopa is reduced, thus increasing its bioavailability in the basal ganglia. Levodopa improves all the clinical symptom of parkinsonism, but does not stop the progression of the disease.

PHARMACOKINETICS:

An oral administration levodopa is rapidly absorbed from the small intestine by an active transport system. Amino acids present in food may interfere with absorption of levodopa hence it should be given 30-60 minutes before meal. Active transport of levodopa into the brain may be inhibited by competition from dietary amino acids. The main metabolic products of levodopa are homovanilic acid(HVA) and 3,4- dihydroxyphenylacetic acid (DOPAC). The metabolites are excreted in urine.

ADVERSE EFFECTS:

  1. GIT: nausea, vomiting, anorexia are common in early treatment with levodopa.
  2. CVS: the commonest cardiovascular side effect is postural hyprtension which is usually asymptomatic. It can also cause tachycardia, palpitation, rarely cardiac arrhythmias.
  3. Abnormal movements: dyskinesia, tics, choreoathetoid movements.
  4. Alteration in smell and taste sensation
  5. Mental changes like insomnia, confusion, delusions, euphoria, depression and nightmares.
  6. Fluctuations in response: after 3-5 years of therapy with progressing disease control becomes poor and fluctuations in symptom occur frequently. Wearing off is due to decrease in plasma concentration of levodopa towards the end of a dose interval. End of dose deterioration can also be improved by administering levodopa in smaller and more frequent doses. THATS ALL ABOUT LEARN ABOUT ANTIPARKINSONIAN DRUGS
Categories
Uncategorized

LEARN ABOUT TUMOURS OF THE LUNG

Tumours of the lung

WHAT IS TUMOUR OF THE LUNG?

A number of benign and malignant tumours occur in the lungs but primary lung cancer commonly termed bronchogenic carcinoma is the most common. The lung is also the commonest site for metastatsis from carcinoma and sarcomas. A histologic classification of various benign and maliganant tumours of the lung are present.

WHAT IS BRONCHOGENIC CARCINOMA?

The term bronchogenic carcinoma is commonly used for cancer of the lungs which includes carcinomonas arising from the respiratory epithelium lining of the bronchi , the bronchioles and alveoli.

WHAT ARE CLASSIFICATION OF LUNG CANCER?

Lung cancer is the most common primary malignant tumour in men and accounts nearly 30% of all the cancer deaths in both sexes in the developing countries. Currently the incidence of lung cancer in females in the UNITED STATES has alresdy exceeded breast cancer as a cause of death in women. Cancer of the lung is a disease of the middle and late life with peak incidence. Of late there has been slight decline in the lung cancer deaths in males due to smoking cessation efforts which started in the males in the west 4 decades back and has started yielding results. However worldwide the scene on its incidence and prognosis are quite grim. Cancer estimate that worldwide by the year 2030 there would be about 10 million deaths per year from lung cancer.

WHAT IS THE CAUSE OF LUNG CANCER?

  1. Smoking: the most important factor for high incidence of all the forms of bronchogenic carcinoma is tobacco smoking. A number of evidences support the positive relationship of lung cancer with tobacco smoking:

i. Total dose: there is adirect statistical correlation between death rate from lung cancer and the total and the amount of cigrattes smoked. Eg:

An average regular smoker has 10 times greater risk of developing lung cancer than a non smoker.

The risk of smokers of more than 2 packs per day fro 20 years is 60-70 times greater than a non smoker.

THATS ALL ABOUT LEARN ABOUT TUMOURS OF THE LUNG.

Categories
Uncategorized

LEARN ABOUT EMPHYSEMA

WHAT IS EMPHYSEMA?

The WHO has defined pulmonary emphysema as combination of permanent dilation of air spaces distal to the terminal bronchioles and the destruction of the walls of dilated air spaces. Thus emphysema is defined morphologically whike chronic bronchitis is defined clinically . since the two conditions co exist frequently and show considerable overlap in their clinical terms, it is usual to label patients as predominant emphysema and predominant bronchitis.

Classification:

According to the portion of acinus involved into 5 types:

  1. Centriacinar
  2. Panacinar
  3. Para septal
  4. Irregular
  5. Mixed

WHAT ARE THE ETIOPATHOGENESIS OF EMPHYSEMA

The component form of COPD is the combination of chronic bronchitis and pulmonary emphysema. Chronic bronchitis however does not always lead to emphysema nor all the cases of emphysema have changes of chronic bronchitis. The association of two conditions is principally linked to the common etiologic factors most important is tobacco smoke and air pollutants.

However pathogenesis of the most significant event is emphysema the destruction of the alveolar walls is not linked to bronchial changes but is closely related to the deficiency of the serum alpha 1- antitrypsin commonly termed protease-antiprotease hypothesis.

Protease- antiprotease hypotheis:

Alpha 1 antitrypsin also called alpha 1 protease inhibitor is a glycoprotein that forms the normal constituent of the alpha 1 globulin fraction of the plasma protein on the serum electrophoresis. The single gen is located in the ong arm of the chromosome 15. It is normally syntheiszed in the liver and is distributed in the circulating blood. The normal function of the alpha 1 antitrypsin is to inhibit protease and hence its name alpha 1 protease inhibitor. The protease are derived from the neutrophils. Neutrophils elastase has the capability of digesting lung parenchyma but is inhibited from doing so by the anti elastase effect of the alpha 1 –AT 1.

Pleura:

WHAT IS PLEURA?

Visceral pleura covers the lung and extends into the fissures while parietal pleura limits the mediastinum and covers the dome of the diaphgram and ineer aspects of the chest wall. The two layers between them enclose pleural cavity which contains less than 15ml of clear serous fluid.

WHAT ARE ITS INFLAMMTIONS?

Its involvement of the pleura is commonly termed pleurities or pleurisy. Depending upon the character of resultant exuduate it can be divided into serous fibrinous and serofibrinous suprative or empysema

  1. Serous fibrinous and sero fibrinous: acute inflammation of the pleural sac can result in serous , serofibrious and fibrious exudate. Most of the cases of such tuberculosis, pneumonias, pulmonary infracts, lung abscess, and bronchiectasis. Other causes include a few collagen disease , uraemia , metastatic involvement of the pleura, irradiation.

Pleurisy causes pain un the chest on breathing and a friction rub is audible on auscultation.

  1. Suppurative pleuritis: bacterial or mycotic infection of the pleura cavity that converts a serofibrious effusion into purulent exudate is termed suppurative pleurities or empyema thoracis. The most common causes is direct spread of pyogenic infection from subdiaphragmatic abscess or liver abscess and penetrating injuries to the chest wall. Occasionally the spread may occur by haematogenous or lymphatic routes.

In empyema the exudate is yellow green creamy pus that accumulates in large volume. Empyema is eventually replaced by granulation tissue and fibrous tissue which obliterate tha cavity and with passage of years calcification may occur. The effect of these is serious respiratory difficulty due to inadequate pulmonary expansion.

3.haemorrhagic pleurities: haemorrhagic pleurities differs from haemthorax in having inflammatory cells or exfoliated tumour cells in the exudate. The causes of haemorrhagic pleuritis are metastatic involvement of the pleura bleeding disorders and rickettsial disease.

Non inflammatory pleural effusion:

1.hydrothorax

2.haemothorax

3.chylothorax

4.pneumothorax

5.spontaneous pneumothorax

THATS ALL ABOUT LEARN ABOUT EMPHYSEMA.

Categories
Uncategorized

WHAT IS ANAEMIA?

WHAT IS ANAEMIA?

Anaemia is defined as a haemoglobin concentration in blood below the lower limit of the normal range for the age and sex of the individual. In adults the lower extreme of the normal haemoglobin is taken as 13.0gm/dl for males and 11.5gm/dl for females. Newborn infants have higher haemoglobin level and therefore 15gm/dl is taken as the lower limit at birth whereas at 3 months the normal lower level is 9.5gm/dl. Although haemoglobin value is employed as the major parameter for determining whether or not anaemia is present the red cells counts haematocrit and absolute values provide alternate means of assessing anaemia.

WHAT ARE PATHOPHYSIOLOGY CAUSE OF ANANEMIA?

Subnormal level of haemoglobin causes lowered oxygen carrying capacity of the blood. This in turn initiates compensatory physiologic adaptations such as follow:

i. Increased release of oxygen from haemoglobin

ii. Increased blood flow to the tissues

iii. Maintenance of the blood volume

iv. Redistribution of blood flow to maintain the cerebral blood supply

Eventually however tissue hyoxia develops causing impaired functions of the affected tissues. The degree of functional impairment of individual tissues is variable depending upon their oxygen requirements. Tissues with high oxygen requirement such as the heart CNS and the skeletal muscle during exercise bear the brunt of clinical effects of anaemia.

WHAT ARE THE CLINICAL FEATURES OF ANAEMIA?

The haemoglobin level at which develops upon 4 main factors:

  1. The speed of onset of anaemia: rapidly progressive t symptom than anaemia of slow onset as there is less time for physiologic adaptation
  2. The severity of anaemia: mild anaemia produces no symptom or signs but rapidly developing severe anaemia may produce significant clinical features.
  3. The age of the patient: the young patient due to good cardiovascular compensation tolerate anaemia quite well as compared to the elderly. The elderly patient develop cardiac and cerebral symptom more prominently due to the associated cardiovascular disease.

WHAT IS SIDEROBLASTIC ANAEMIA?

The sideroblastic anaemia comprise a group of disorders of diverse etiology in which the nucleated erythroid precursors in the bone marrow show characterstics ‘ringed sideroblastic,.

WHAT ARE SIDEROCYTES AND SIDEROBLATS?

Siderocyctes and sideroblasts are erythrocytes and normoblasts respectively which contain cytoplasmic granules of iron.

WHAT IS MEANT BY SIDEROCYCTES?

these are red cells containing granules of non-haem iron. These granules stain positively with Prussian blue reaction as well as stain with Romanowsky dyes when they are referred to as pappenheimer bodies. Siderocytes are normally not present in the human appear following spelenectomy. This is because the reticulocytes on release from the marrow are finally sequestered in the spleen to become matured red cells. In the absence of spleen the final maturation step takes place in the peripheral blood and hence siderocytes make their appearance in the blood after splenectomy.

WHAT IS MEANT BY SIDEROBLASTS?

these are nucleated red cells containing sideroblastic granules which stain positively with Prussian blue reaction. Depending upon the number size and distribution of sideroblastic granules, sideroblasts may be normal or abnormal.

Normal sideroblats contain a few fine scattered cytoplasmic granules representing iron which has not been utilised for haemoglobin synthesis. These cells comprise 30-50% of normoblasts in the normal marrow but are reduced or absent in iron deficiency.

Abnormal sideroblasts are further of 2 types:

One type is a sideroblast containing numerous diffusely scattered a coarse cytoplasmic granules and are seen in conditions such as dyserythropoiesis and haemolysis. In this type, there is no defect of haem or globin synthesis but the percentage saturation of transferrin is increased.

The other is ringed sideroblast in which haem synthesis is disturbed as occurs in sideroblasts anaemia. Ringed sideroblasts in which haem synthesis. The ringed arrangement of these granules is due to the presence of iron-laden mitochondria around the nucleus.

WHAT ARE THE TYPES SIDEROBASTIC ANAEMIA?

Hereditary sideroblastic anaemia

Acquired siceroblastic anaemia

THATS ALL ABOUT” WHAT IS ANAEMIA?” .

Categories
Uncategorized

LEARN ABOUT TREATMENT OF GIT DISEASE

LEARN ABOUT TREATMENT OF GIT DISEASE

DRUG USED IN THE TREATMENT OF GASTROINTESTINAL DISEASE

Nausea and vomiting are protective reflexes that help to remove toxic substances from the gastrointestinal tract. They are the symptoms of altered function but are not disease. Nausea denotes the feeling of impending vomiting, whereas vomiting refers to the forceful expulsion of the contents of the stomach and upper intestinal tract through the mouth. Retching is he laboured rhythmic respiratory activity which usually preceeds vomiting.

The act of vomiting is controlled by the vomiting centre in the medulla. Stimuli are relayed to this centre from peripheral areas that is gastric mucuosa and other parts of GIT. Sensory stimuli also arise within the central nervous system itself – the impulses are transmitted to the vomiting centre.

The lack of blood brain barrier at the chemoreceptor trigger zone allows it to be directly stimulated by blood borne drugs and toxic substances. Nausea and vomiting may be the symptoms of pregnancy, serious organic substances of almost any of the viscera or may be produced by infection, drugs, radiation, painful stimuli motion sickness metabolic and emotional distrubances. The main neurotransmitter involved in the control of vomiting are acetylcholine histamine 5-hydroxytryptamine and dopamine.

EMETICS

The drugs that cause vomiting are called emetics. Eg mustard, common salt, ipeac, and apomorphine. Mustard and common salt are commonly used household emetics. Syrup ipeac is a safer emetic than apomorphine. Emetics are indicated in certain case of poisoning.

Contraindications for the use of emetics are:

  1. Children
  2. Unconscious patients
  3. Corrosive and caustic poisoning
  4. Poisoning due to CNS stimulants
  5. Kerosene poisoning

ANTIMETICS

The drugs that are used to prevent or control vomiting are called antiemetics.

CLASSIFICATION

  1. Anticholinergics: scolpolamine, dicyclomine
  2. Antihistamine(h1 blockers): dimenhydrinate, diphenhydramine, cyclizine, meclizine, hydroxyzine
  3. 5-HT3 receptor anatagonist: ondansetron, dolasetron, palonosetron
  4. Prokinetic agents: metoclopramide, domperidone

THATS ALL ABOUT LEARN ABOUT TREATMENT OF GIT DISEASE . HOPE YOU LIKE THE TOPIC. PLEASE COMMENT DOWN BELOW AND SHARE THE POST.

Categories
Uncategorized

DIURETICS

DIURETICS
DIURETICS

diuretics are the drugs which cause a net loss of sodium and water in urine. However, sodium balance is soon restored even with continuing diuretics action by compensatory homeostatic mechanism of the body.

Application of the diuretic in the management of hypertension, has outstriped their use in edema. Diuretics has also helped in understanding renal pharmacology.

CLASSIFICATION:

1.HIGH EFFICACY DIURETICS: furosemide, bumetamide, torsemide

  1. MEDIUM EFFICACY DIURETICS:

a. thiazide: hydrochlorothiazide, benzthiazide, chlorothiazide ,hydroflumethiazide

b. thiazide related drugs: chlorthalidone, metolazone,indapamide, clopamide.

  1. WEAK OR ADJUNCTIVE DIURETICS:

a. carbonic anhydrase inhibitor: acetazolamide

b. potassium sparing diuretics: spironolactone, eplerenone, amiloride, triamterene

c. osmotic diuretics: mannintol, glycerol, isosorbid

  1. HIGH CEILING DIURETICS:

furosemide: the diuretics response gets on increasing with increasing dose upto 10l of urine may be produced in a day. it is active even in patients with relatively severe renal failure.

major site of action is thick ascending loop of henle where furosemide inhibits sodium-potassium-2chlorine transport.

furosemide has weak carbonic anhydrase inhibiting action ,increased HCO3 excretion, as well urinary pH may rise but the predominant urinary action is chlorine.therefore acidosis does not develop . the diuretics action is independent of acid-base balance of the body.

furosemide increase calcium excretion as well as magnesium excretion by abolishing transepithelial potential difference in the thick ascending loop of henle which drives reabsorption of the divalent cations.

bumetamide: similar to furosemide but 40 times more potent. hyperuricaemia ,k+ loss, glucose intolerance and toxicity are less marked but it rarely cause myopathy.

therapeutic uses:

  1. during the inital stages of renal, hepatic and cardiac odema loop duretics are preferred.
  2. intravenous furosemide is used in hypercalcaemia as it promotes the excretion of calcium in urine.
  3. acute pulmonary oedema
  4. loop diuretic may be used in cerebral oedema, but i.v. mannintol is the preferred drug, in hypertensive emergencies. furosemide is not preferred in uncomplicated primary hypertension because of short duration of action.

5.loop diuretics can be used in mild hyperkalaemia.

ADVERSE REACTION:

1.electrolyte disturbance: hypokalaemia, hyponatraemia, hypokalaemic metabolic alkalosis, hypocalcaemia and hypomagnesia

  1. metabolic disturbances: hyperglycaemia, hyperlipidaemia, hyperuricaemia.
  2. ototoxicity manifests deafness, vertigo, and tinnitus. the symptoms are usually reversible on stoppage of therapy.

DRUG INTEREACTION:

  1. furosemide with digoxin: these diuretic cause hypokalaemia which increase the binding of digoxin to sodium and potassium ATPase leading to digoxin toxicity.
  2. furosemide with aminoglycoside: both are ototoxic drugs and cause enhanced toxicity when use together.
  3. furosemide with nonsteroidal antiinflammatory: non seroidal antiinflammatory drugs inhibit PG synthesis and block postaglandin mediated haaemodynamic changes of loop diuretics.
  4. furosemide with amiloride; furosemide cause hypokalaemia whereas amiloride conserve potassium.

2.MEDIUM EFFICACY DIURETICS:

thiazides and related diuretics:

chlorothiazide was synthesized a carbonic anhydrase inhibitor variant which produces urine that was rich in chloride and diuresis ocurred in alkalosis aw well as acidosis.

the medium efficacy diuretics with primary site if action in the cortical diluting segment or the early distal tubes. here they inhibit sodium and chloride symport at the luminal membrane. they donot effect the corticomedullary osmotic gradient indicating lack of action at the medullary thick ascending loop of henle.

by their action to reduce blood volume as well as intrarenal haemodynamic change they tend to reduce glomerular filtration rate.

chlorthalidone: long acting compound.

metolaone: common with loop diuretics. it is able to evoke a clinically usefusl

USES:

1.hypertension: thiazides are used in the treatment of essential hypertension

  1. heart failure : thiazides are used for mild to moderate case of heart failure
  2. hypercalciuria: thiazides are used in calcium nephrolithiasis as they reduce the urinary excretion of calcium.
  3. diabetes insipidus:
  4. WEAK OR ADJUNCTIVE DIURESIS;

A. SPIRONOLACTONE:

it is a aldosterone antagonist . aldosterone bind to specific mineralocorticoid receptor in the cytoplasm of the late distal tubule and collecting duct cells. spironolactone is most effective when circulating aldosterone levels are high. it also increase calcium excretion.

USE;

  1. odematous conditions associated with secondary hyperaldosteronism.
  2. spironolactone is often used with thiazides to compensate potassium loss.

DRUG INTEREACTION:

ACE inhibitors with spironolactone : dangerous hyperkalemia can occur.

AMILORIDE AND TRIAMTERENE:

they directly block the sodium channels in the luminal membrane of the cells of the late DCT and CD cells.

USES:

  1. treatment of hypertension
  2. treatment of lithium induced nephrogenic diabetes insipidus
  3. amiloride improves mucociliary clerance in patients with cystic fibrosis.

B. CARBONIC ANHYDRASE INHIBITOR:

it function in co2 and HCO3 transport and H + ion secretion. the enzyme is present in renal tubular cell, gastric mucosa etc.

ACETAZOLAMIDE:

uses:

  1. glaucoma

2.alkalinize urine in acidic drug poisoning

  1. acute mountain sickness

ADVERSE EFFFECTS:

hypersensitivity reactions, drowsiness, paraesthesia, hypokaemia, metabolic acidosis , headache etc.

CONTRADICTIONS: liver diseae and chronic obstructive pulmonary disease

C. OSMOTIC DIURETICS:

MANNINTOL: adminstered i.v. . it is neither metabolized in the body nor reabsorbed from the renal tubules.

USES:

  1. shock, renal shutdown, cardiovascular surgery, haemolytic transfusion
  2. reduce elevated intracranial tension

3.acute congestive glaucoma.

Categories
Uncategorized

THINGS YOU SHOULD KNOW ABOUT ANTI-DEPRESSANTS

THINGS YOU SHOULD KNOW ABOUT ANTI-DEPRESSANTS
Things you should know about ANTI_DEPRESSANTS

Depression is a very common clinical condition. it is associated with the feeling of sadness, loss of interest, self neglect, anorexia, sleep disturbances, suicidal feeling in severe cases etc.

various hypothesis have been proposed for pathogenesis of depression:

  • decrease in levels or function of monoamines in cortical and limbic system.
  • decrease in brain derived neurotrophic factor
  • abnormalities in HPA axis, thyroid function and sex steroids level.

Antidepressants are drugs which can elevate mood in depression illness. practically, all antidepressants affect monoaminergic, transmission in the brain in one way or the other and many of them have other associated properties.

CLASSIFICATION:

  1. tricyclic antidepressants : amitriptyline, amoxapine, doxepine, trimipramine, imipramine, clopmipramine
  2. selective serotonin reuptake inhibitors :fluoxentine, fluvoxamine, citalopram, sertaline, paroxetine.
  3. atypical antidepressants: trazodone, bupropion, , mirtazapine, venlafaxine,
  4. MAO-A inhibitors: moclobemide, clorgyline.

TRICYCLIC ANTIDEPRESSANTS:

tricyclic antidepressants are well absorbed through the GI tract and are highly bound to plasma proteins. they are widely distributed in tissue including CNS. they are metabolized in liver. some of them like imipramine, amitriptyline etc produce active metabolite which are responsible for the long duration of action of these drugs.

Adverse effects and contradictions of tricyclic antidepressants:

  1. atropine like side effects : dryness of mouth, blurring of vision, constipation, urinary retention
  2. alpha-1 adrenergic blocking effects: postural hypotension, tachycardia, cardiac arrhythmias ,
  3. H-1 blocking effects: sedation and confusion
  4. other effects: increased appetite, weight gain, and may precipitate convulsions.

mechanism of action of antidepressants
mechanism of action of tricyclic antidepressants

MAO INHIBITORS:

MAO is a mitochondrial enzyme involved in the metabolism of biogenic amines. there are two isoforms of MAO . MAO is responsible mainly for the metabolism of NA 5-HT and tyramine. MAO-B selective for dopamine metabolism.

MOCLOBEMIDE

a selective and reversible inhibitor of MAO-A is relatively free of food and drug intereactions. hence,cheese reaction is rare. it is also devoid of anticholinergic , alpha-1 adrenergic blocking and sedative effects.

DRUG INTEREACTIONS:

  1. tricyclic antidepressants involves hypertensive crisis, hyperpyrexia, convulsions, coma

serotonin syndrome: concomitant adminsitration of SSRIs with MAO inhibitors produce severe undesirable effects like tremor, restlessness, muscle rigidity, hyperthermia, sweating, seziures, coma due to increased serotonin levels at the synapse which is termed srotonin syndrome.

  1. SSRIs inhibit metabolism of a number of drugs such as antipsychotics, beta blockers , phenytonin etc can increase their plasma levels.

CHEESE REACTION

USES OF ANTI DERPRESSANTS:

  1. depression: antidepressants are used in the treatment of bipolar illness. it is better tolerability, less side effects .
  2. panic disorders
  3. obsessive compulsive disorders
  4. nocturnal enuresis
  5. atopic dermatitis.
Categories
Uncategorized

USES OF ANTIHISTAMINES

USES OF ANTIHISTAMINES

Anticholinergic

Scopolamine is the drug of choice to prevent motion sickness. It blocks afferent impulses from vestibular apparatus to the vomiting centre by its anticholinergic action. Its sedative effect also contributes to its antiemetic effect. Scopolamine is not effective for other types of vomiting.

ANTIHISTAMINES (H-1 BLOCKERS)

h-1 blockers are mainly useful for the prevention of motion sickness. They are also effective in morning sickness, postoperative and other types of vomiting. Dimenhdyrinate, diphenhydramine, doxylamine, promethazine, cyclizine, and meclizine are some of the h-1 blockers that are antiemetic properties. Their antiemetic effect is due to sedative and central anticholinergic actions. Cyclizine and meclizine have less sedative effect. Meclizine has longer duration of action.

5-HT3-RECEPTOR ANTAGONIST

Ondasetron is the prototype drug. Other drug are granisetron, dolasetron, and palonosetron. Their antiemetic effect is mainly due to the blockade of 5-HT3 receptors on vagal afferents in the gut. In addition they also block 5-HT 3 receptors in the CTZ and solitary tract nucleus(STN).

Ondansetron and other 5-HT3 antagonist control vomiting by blocking enetogenic impulses in the gut and their central relay.

PHARMACOKINETICS

5-HT 3 antagonist are well absorbed after oral administration –ondansetron undergoes extensive first pass metabolism. The metabolites are excreted in urine and facecs. These agents are also available for intravenous administration. Ondansetron can also be administred intramuscularly. Granisetron is more potent and longer acting than ondasetron. Transdermal patch of granisetron is available for prevention of cancer chemotherapy induced vomiting. Palonosetron has the longest duration of action among the 5-HT3 antagonist.

USES OF ANTIHISTAMINES

  1. 5-HT 3 antagonist re the most effective agent for prevention and treatment of anti-cancer drug induced nausea and vomiting.
  2. They are also effective in hyperemesis of pregnancy postoperative and postradiation vomiting but they are ineffective against motion sickness.

ADVERSE EFFECTS

5-HT3 antagonist are well tolerated. They may cause headache , dizziness and diarrhoea.

THATS ALL ABOUT USES OF ANTIHISTAMINES.HOPE YOU ALL FIND THIS TOPIC USEFUL.

Categories
Uncategorized

Hello world!

Welcome to WordPress. This is your first post. Edit or delete it, then start writing!