1.
PHARMACOLOGY IMPORTANT
LONG QUESTIONS (15 MARKS)
(PART 2: QUESTION NO. 8-14)
PREPARED
BY MR. ABHIJIT DAS
1.
What do you mean by parenteral route?
What are advantages of parenteral routes over oral route? Classify parenteral
route.
2. Define
absorption of drugs. Give a note on different processes of absorption of drugs
and factors affecting the absorption process.
3. Define
biotransformation of a drug. Describe various processes of drug metabolism.
4. Explain
the various factors affecting the dose and action of drugs.
5. Define
cholinergic drugs. Classify it with suitable suitable examples. Give a note on
pharmacological action of acetylcholine.
6. What
do you mean by sympathomimetics and parasympathomimetics? Classify
anti-cholinergic drugs. Discuss pharmacological action of atropine on eye, CVS,
glands and smooth muscles.
7. Define
adrenergic drugs & classify them. Describe about pharmacological action,
adverse effect and use of adrenaline.
8. Write
down the definition, classification, mechanism of action, pharmacological
action and use of local anaesthetics.
9. Explain
general anaesthetics. Briefly describe the different stages of general
anaesthesia. Write a note on barbiturates.
10.
What are NSAIDS? Classify them. Write
the mechanism of action, pharmacological action and uses of aspirin.
11.
what is the difference between narcotic
and non-narcotic analgesics? Classify opiod
analgesics. Give a note on pharmacological actions, ADME, side effects
and therapeutic effects of morphine.
12.
Define epilepsy. Describe shortly
different types of epilepsy. Classify anti epileptic drugs. Write the mechanism
of action and adverse effects of phenytoin.
13.
What is sedative? Classify the drugs
used as sedative-hypnotics. Give an account of pharmacological action, ADME,
adverse reactions and therapeutic uses of barbiturates.
14.
Define diuretics. Classify it. Write
down the pharmacological action, adverse effect and use of furosemide.
15.
What do you mean by cardiac glycosides?
Write the mechanism of action, pharmacological action, adverse effects and uses
of digoxin.
16.
Enumerate the drugs used for the
treatment of peptic ulcer and describe pharmacological action, toxicities of H2
blockers.
17.
What is purgative? Classify it with
example. Give a note on irritant purgatives.
18.
Define chemotherapeutic agents and
antibiotics. Write the mechanism of action of penicillins and a note on
semi-synthetic penicillins. Or Classify penicillins and describe their method
of action, toxicity and therapeutic uses.
19.
What is tuberculosis? Classify anti
tubercular drugs with examples. Give a note on firstline anti tubercular drugs.
20.
What is amoebiasis? Classify antiamoebic
drugs. Discuss about the mechanism of action, pharmacokinetics, side effects
and uses of metronidazole.
21.
What is cancer? Classify anti cancer
drugs. Discuss shortly the mechanism of action of anti metabolites and
alkylating agents.
8. WRITE DOWN THE DEFINITION, CLASSIFICATION, MECHANISM OF ACTION,
PHARMACOLOGICAL ACTION AND USE OF LOCAL ANAESTHETICS.
ANS:
LOCAL ANAESTHETICS
Local anaesthetics,
excepting some special instance, act on peripheral nerves. Therefore we study
local anaesthetics and general anaesthetics separately.
Local anaesthetics,
being applied topically or injected locally, cause
reversible loss of pain sensation in a localized area.
Local anaesthetics
are safer than general anaesthetics because consciousness is not lost with them
and functions of heart, lungs, liver etc are not affected.
However, with many
major surgeries, local anaesthetics are not suitable.
CLASSIFICATION OF DRUGS
INJECTABLE ANAESTHETICS
LOW POTENCY, SHORT
DURATION: Procaine, Chloroprocaine
INTERMEDIATE
POTENCY: Lidocaine (Lignocaine), Prilocaine
HIGH POTENCY, LONG DURATION: Tetracaine, Bupivacaine, Ropivacaine, Dibucaine
SURFACE ANAESTHETICS
SOLUBLE: Cocaine,
Lidocaine, Tetracaine, Benoxinate
INSOLUBLE:
Benzocaine, Oxethazaine, Butylaminobenzoate
MECHANISM OF ACTION
Local anaesthetics reversibly inhibit nerve
transmission by binding to voltage-gated sodium channels in the nerve plasma
membrane (by preventing depolarization).
Therefore they prevent the development of
action potential in the nerve fibre.
PHARMACOLOGICAL ACTION
EFFECT OF SENSATION
They block the sensation of pain, then they block the sensation for touch and pressure.They produce blockade of both small and large nerve fibres.
CNS
They produce stimulation of CNS. That’s why
they produce euphoria.
Cocaine is a powerful CNS stimulant which also
causes euphoria, excitement, mental confusion, restlessness and tremor.
Procaine and other synthetic LAs are much less
potent. At higher doses they produce CNS stimulation followed by depression.
CARDIOVASCULAR SYSTEM
They produce vasodilation(Hypotension) but cocaine produce
vasoconstriction(Hypertension).
They produce depressant effect on the
myocardium.
LAs tend to fall in blood pressure.
SMOOTH MUSCLE
They produce relaxant effect on smooth
muscles.
ADVERSE
EFFECTS
1. Dizziness
2. Headaches
3. Blurred vision
4. Twitching muscles
5. Weakness
6. Continuing numbness
7. Allergic reaction
THERAPEUTIC USES
1. Surface anaesthesia for pain.
2. Used as local infiltration anaesthesia
3. Used as antiarrhythmic agents
4. LAs are used for procedures such as performing
a skin biopsy, repairing a broken bone, stiching a deep cut etc.
9. EXPLAIN GENERAL ANAESTHETICS.
BRIEFLY DESCRIBE THE DIFFERENT STAGES OF GENERAL ANAESTHESIA. WRITE A NOTE ON
BARBITURATES.
ANS:
GENERAL ANAESTHETICS
General anaesthetics
are drugs which produce reversible loss of all sensation and consciousness. The
features of general anaesthesia are:
Ø Analgesia
Ø Unconsciousness
Ø Amnesia
Ø Loss
of sensation and ANS reflexes
Ø Skeletal
muscle relaxation
Each of these features
are reversible.
STAGES OF ANAESTHESIA
STAGE I
In this stage pain
disappears, hence this stage is called stage of analgesia. This stage is
produced because at this stage, a transmission block appears so carriage of
pain sensation is blocked.
STAGE II
In this stage patient
becomes agitated and violent. Blood pressure of the patient rises, respiratory
rate becomes rapid and respiration is often irregular. This stage may be
dangerous for the patient.
STAGE III
This stage is called stage of surgical anaesthesia
because surgery is undertaken at this stage. In this stage respiration becomes
regular and skeletal muscles relax.
STAGE IV
In this stage the
respiratory centre in the medulla is depressed so stoppage of respiration
occurs. If not checked properly, then death can happen.
CLASSIFICATION OF
GENERAL ANAESTHETICS
1.
INHALATION ANAESTHETICS: Ether,
Chloroform, Halothane, Enflurane,
Cyclopropane, Nitrous Oxide
2.
INTRAVENOUS ANAESTHETICS:
A. INDUCING
AGENTS: Thiopental, Methohexital, Propofol, Etomidate
B. SLOWER ACTING AGENTS: Diazepam, Lorazepam, Midazolam
MECHANISM OF ACTION OF
GENERAL ANAESTHETICS
The mechanism of action
of GAs are not fully understood yet. They don’t act on specific receptors.
The GAs are lipid soluble. That’s why they enter into the cell membrane of the neurons. This results in some disturbance of the neurons and is called fludization. Fluidization inhibits the entry of NA+ channel into the cell membrane which leads to inhibition of depolarization of the neurons(So pain signals can not be transmitted).
BARBITURATES AS
ANAESTHETICS
Barbiturates such as
thiopental, methohexital etc are used as GAs. Because they induce
unconsciousness extremely rapidly.
THIOPENTAL
After IV injection
thiopental reaches the brain quickly because brain is richly perfused by blood.
Thiopental is very lipid soluble, crosses the blood brain barrier quickly and
is dissolved in brain so unconsciousness develops.
ADVERSE EFFECT
Ø Laryngospasm
Ø Respiratory
depression
Ø Hypotension
USES
1.
As inducing agent for GA
2.
For some short duration surgical
procedure
METHOHEXITAL
it
Is similar to thiopental. It is three times more potent than thiopentone
and has a quicker and briefer action.
10.
WHAT ARE NSAIDs? CLASSIFY THEM. WRITE THE MECHANISM OF ACTION,
PHARMACOLOGICAL ACTION AND USES OF ASPIRIN.
ANS:
NSAIDs
Ø Non-steroidal anti-inflammatory drugs
(NSAIDs) are drugs that are commonly used to bring down a high temperature,
relieve pain, and reduce inflammation.
Ø They are used to relieve symptoms of headaches, colds and flu, arthritis, and
other causes of long-term pain.
Ø They are not steroids (steroids, also called
as corticosteroids, are man- made version of chemicals used to treat
inflammation).
CLASSIFICATION
A.
NONSELECTIVE
COX INHIBITORS
1.
Salicylates:
Aspirin.
2.
Propionic
acid derivatives: Ibuprofen, Naproxen, Ketoprofen, Flurbiprofen.
3.
Anthranilic
acid derivative: Mephenamic acid.
4.
Aryl-acetic
acid derivatives: Diclofenac, Aceclofenac.
5.
Oxicam
derivatives: Piroxicam, Tenoxicam.
6.
Pyrrolo-pyrrole
derivative: Kitorolac.
7.
Indole
derivative: Indomethacin.
8.
Pyrazolone
derivatives: Phenylbutazone, oxyphenbutazone.
B.
SELECTIVE
COX-2 INHIBITORS: Celecoxib, Parecoxib, Etoricoxib.
C.
ANALGESIC-ANTIPYRETICS
WITH POOR ANTI-INFLAMMATORY ACTION
1.
Paraaminophenol
derivative: Paracetamol (Acetaminophen).
2.
Pyrazolone
derivatives: Metamizol (Dipyrone), Propiphenazone.
3.
Benzoxazocine:
Nefopam
MECHANISM OF ACTION OF NSAIDS
The mechanism of action of
NSAIDs is the inhibition of the enzyme cyclooxygenase (COX).
Cyclooxygenase is required to convert arachidonic acid into thromboxanes (TXA2),
Prostacyclins (PGI2), and Prostaglandins (PGE2).
Thromboxane is responsible for platelet aggregation, prostacyclin is
responsible for gastric protection and
prostaglandin is responsible for pain, fever and inflammation.
So NSAIDs inhibit production of prostaglandins, a group of compounds
that contribute to inflammatory response and are responsible for signs such as
fever and pain.
ASPIRIN
Aspirin is acetylsalicylic acid. It is rapidly converted in the body
to salicylic acid which is responsible for most of the actions.
MECHANISM OF ACTION
Aspirin non-selectively inhibits COX enzyme that means aspirin inhibits
both COX-1 and COX-2. So ultimately PGE2 biosynthesis is inhibited, which was
responsible for pain, fever, and inflammation.
PHARMACOLOGICAL ACTIONS
1. METABOLIC EFFECTS
Cellular metabolism is increased in skeletal muscles. So increased
utilization of glucose is observed and blood sugar may decrease and liver
glycogen is depleted.
2. RESPIRATION
At anti-inflammatory doses, respiration is stimulated. Further rise in
salicylate level causes respiratory depression which may lead to death due to
respiratory failure
3. CVS (CARDIO VASCULAR SYSTEM)
Larger doses of aspirin increase cardiac output to meet increased
peripheral oxygen demand and cause direct vasodilation so Blood pressure may
fall.
4. GIT (GASTRO INTESTINAL TRACT)
Aspirin irritates gastric mucosa, causes nausea and vomiting.
Aspirin also causes acute ulcer and erosive gastritis.
5. BLOOD
Aspirin, even in small doses, irreversibly inhibits TXA2. So aspirin
interferes with platelet aggregation and bleeding time is prolonged to nearly
twice the normal value.
6. IMMUNOLOGICAL EFFECT
Aspirin inhibits antigen-antibody reaction.
ADVERSE EFFECTS
1.
At
analgesic dose aspirin causes nausea, vomiting, blood loss in stools, peptic
ulcer etc.
2.
Skin
rashes of various types.
3.
Bone
marrow depression leading to anaemia.
4.
Hypersensitivity
reactions such as angioedema (painless swelling under the skin), asthma, and
anaphylaxis (severe life-threatening allergic reaction).
5. Dizziness, tinnitus (ringing or buzzing noise in one or both ears).
THERAPEUTIC USES
1.
As
analgesic for headache, backache, joint pain, tooth ache etc.
2.
As antipyretic
against fever of any origin. Paracetamol, being safer, is generally preferred.
3.
Used in
acute rheumatic fever.
4.
Used in
Rheumatoid arthritis.
5.
Used in
Osteoartthritis.
6.
Used in
postmyocardial infraction patients by inhibiting platelet aggregation.
11.
WHAT IS THE DIFFERENCE
BETWEEN NARCOTIC AND NON-NARCOTIC ANALGESICS? CLASSIFY OPIOD ANALGESICS. GIVE A NOTE ON PHARMACOLOGICAL
ACTIONS, ADME, SIDE EFFECTS AND THERAPEUTIC EFFECTS OF MORPHINE.
ANS:
DIFFERENCE BETWEEN NARCOTIC AND NON-NARCOTIC
ANALGESIC
|
NARCOTICS |
NON-NARCOTICS |
|
Ø These are opioid analgesics Ø They act centrally Ø They are habit forming Ø They can be natural or synthetic Ø Ex: Morphine, Heroine |
Ø These are non-steroidal-anti-inflammatory
drugs (NSAIDs) Ø They act peripherally Ø They are not habit forming Ø They are all synthetic Ø Ex: Ibuprofen, Paracetamol |
CLASSIFICATION OF OPIOID ANALGESICS
1.
NATURAL
OPIUM ALKALOIDS
a.
Phenanthrene
derivatives: Morphine, Codeine, Thebaine
b.
Benzylisoquinoline
derivatives: Papaverine, Noscapine
2.
SEMISYNTHETIC
DERIVATIVES OF OPIUM ALKALOIDS: Heroine, Apomorphine
3.
SYNTHETIC
SUBSTITUTES OF OPIUM ALKALOIDS: Pentazocine, Pethidine, Methadone
MORPHINE
Morphine is the principal alkaloid in opium.
PHARMACOLOGICAL ACTIONS OF MORPHINE
CNS
Morphine reduces poorly localized visceral pain in a better way than
sharply defined somatic pain. Higher doses can reduce even severe pain.
Morphine has sedative nature and can cause drowsiness.
Patients in pain or anxiety, and especially addicts, perceive it as pleasurable
floating sensation.
RESPIRATION
Morphine depresses respiratory centre. Respiration rate is decreased.
Death in morphine poisoning is due to respiratory failure.
CARDIO VASCULAR SYSTEM
Morphine causes vasodilation and fall of blood pressure.
Morphine also causes bradycardia due to stimulation of vagal centre.
Cardiac work is consistently reduced.
GIT
Morphine increases the tone of smooth muscles and decreases GI
motility which causes constipation.
Morphine also decreases GI secretions.
SMOOTH MUSCLES
Morphine causes contraction of urinary bladder and ureter.
Morphine releases histamine which causes bronchoconstriction.
NEURO ENDOCRINE
Morphine inhibits GnRH (Gonadotrophin releasing hormone) secretion.
Morphine also inhibits CRH (corticotropin releasing hormone) secretion. As a result FSH, LH levels are lowered.
ADME (OR PHARMACOKINETICS)
ABSORPTION: Morphine is well absorbed through parenteral route (IV,
SC, IM).
DISTRIBUTION: widely distributed to liver, kidney and spleen.
METABOLISM: Morphine is metabolized in liver by glucoronide
conjugation.
ELIMINATION: elimination is almost complete in 24 hours via urine.
ADVERSE EFFECTS
1.
Respiratory
depression can happen. Death due to morphine poisoning is due to respiratory
depression.
2.
Mental
confusion and sedation can happen in CNS.
3.
Hypotension
(decreased blood pressure)
4.
Tolerance
and dependence can happen.
5.
Allergic
reaction: a local reaction may appear at injection site due to histamine
release. Swelling of lips can be seen.
THERAPEUTIC USES
1.
It is
used as an analgesic agent. It acts in severe constant pain rather than sharp
intermittent pain.
Chronic pain due to terminal stage of cancer is usually treated with
morphine.
2.
Morphine
is used to treat pulmonary edema.
3.
It is
used as a preanaesthetic drug.
4.
Morphine
is used as an antitussive agent (suppress ciugh).
5.
Morphine
is also used to treat diarrhea as it produces constipation.
12.
DEFINE EPILEPSY. DESCRIBE SHORTLY DIFFERENT TYPES OF EPILEPSY.
CLASSIFY ANTI EPILEPTIC DRUGS. WRITE THE MECHANISM OF ACTION AND ADVERSE
EFFECTS OF PHENYTOIN.
ANS:
EPILEPSY
Epilepsy is a CNS disorder in which brain activity becomes abnormal,
causing seizures or periods of unusual behavior and sometimes loss of
awareness.
SEIZURE
A seizure is an abnormal electrical activity in the brain that happens
quickly.
TYPES OF EPILEPSY
1.
GENERALIZED
SEIZURES: Affect both sides of the brain
A.
GENERALIZED
TONIC-CLONIC SEIZURES
It is also called as Grand mal seizures. It can make a person cry out,
lose consciousness, fall to the ground etc.
B.
ABSENCE
SEIZURES
It is also called as petit mal seizures. It can cause rapid blinking
on a few seconds of staring into space.
C.
ATONIC
SEIZURES
Unconsciousness with relaxation of all muscles due to excessive
inhibitory discharges.
D.
MYOCLONIC
SEIZURES
Shock like momentary contraction of muscles of a limb or the whole
body.
2.
FOCAL
SEIZURES/PARTIAL SEIZURES: Affect only one side of the brain
A.
SIMPLE
PARTIAL SEIZURES
These affect a small part of the brain. These seizures can cause
twitching or a change in sensation, such as a strange taste or smell.
B.
COMPLEX
PARTIAL SEIZURES
It can make a person confused. The person will be unable to respond to
questions for up to a few minutes.
C.
SECONDARY
GENERALIZED SEIZURES
It begins in one part of the brain, but then spreads to both sides of
the brain.
In other words, the person first has a focal seizure and then a generalized seizure.
CLASSIFICATION OF ANTIEPILEPTIC DRUGS
1.
Barbiturate:
Phenobarbitone
2.
Deoxybarbiturate:
Primidone
3.
Hydantoin:
Phenytoin, Fosphenytoin
4.
Iminostilbene:
Carbamazepine, Oxcarbazepine
5.
Succinimide:
Ethosuximide
6.
Aliphatic
carboxylic acid: Valproic acid, Divalproex
7.
Benzodiazepines:
Clonazepam, Diazepam, Lorazepam, Clobazam
8.
Phenyltriazine:
Lamotrigine
9.
Cyclic
GABA analogue: Gabapentin
10. Newer drugs: Vigabatrin, Topiramate, Tiagabine, Zonisamide, Levetiracetam
PHENYTOIN
It is a synthetic compound related to hydration.
It is used to treat epilepsy. Phenytoin is available on prescription.
It comes as tablets that can be chewed or dissolved in water. It also comes as
capsules and a liquid that can be swallowed.
MECHANISM OF ACTION OF PHENYTOIN
Entry of Na+ ions via Na+ ion channels cause
depolarization of neuron in the brain.
Phenytoin blocks the Na+ entry in the brain neurons which
are repetitively producing action potentials in rapid rate.
This action of phenytoin is thus a ‘membrane stabilizing action’ and it acts on those neurons which are overworking.
ADVERSE EFFECTS
1.
CNS
depression
2.
Confusion,
drowsiness and hallucination can occur.
3.
Gum
Hypertrophy
(Hypertrophy: enlargement of an organ or tissue in size)
4.
Megaloblastic
anaemia
(large RBCs and a decrease in the number of RBCs)
5.
Vitamin
D deficiency which can lead to rickets.
6.
Hyperglycemia
can occur.
7.
Teratogenic
effect of Phenytoin-Phenytoin Intake during pregnancy can lead to teratogenic
effects characterized by congenital heart disease and mental defect.
USES
Ø Phenytoin is used to treat generalized
tonic-clonic seizures
Ø It is also used to treat both simple and
complex partial seizures.
13. WHAT IS SEDATIVE? CLASSIFY THE DRUGS USED AS SEDATIVE-HYPNOTICS. GIVE AN ACCOUNT OF PHARMACOLOGICAL ACTION, ADME, ADVERSE REACTIONS AND THERAPEUTIC USES OF BARBITURATES
ANS:
Sedatives are a group of drug that slow down brain activity without
inducing sleep. These drugs are prescribed to help patients calm down, feel
more relaxed and get better sleep.
Hypnotics are a group of drugs that induce sleep and reduce wakefulness during sleep.
CLASSIFICATION
BARBITURATES
LONG ACTING: Phenobarbitone
SHORT ACTING: Butobarbitone, Phentobarbitone
ULTRA-SHORT-ACTING: Thiopentone, Methohexitone
BENZODIAZEPINES
HYPNOTIC: Diazepam, Flurazepam, Nitrazepam, Alprazolam, Temazepam,
Triazolam
ANTIANXIETY: Diazepam, Chlordiazepoxide, Oxazepam, Lorazepam,
Alprazolam
ANTICONVULSANT: Diazepam, Lorazepam, Clonazepam, Clobazam
NEWER NONBENZODIAZEPIN HYPNOTICS: Zopiclone, Zolpidem, Zaleplon
BARBITURATES
Today barbiturates are not used to promote sleep or to calm patients
because they are not safe drugs.
Barbiturates are substituted derivatives of barbituric acid.
Barbiturates have variable lipid solubility, the more soluble ones are
more potent.
MECHANISM OF ACTION OF BARBITURATES
When GABA binds to its receptors, the Cl- channel opens and
Cl- ions enter into the post synaptic neuron and as a result the
post synaptic neuron is hyperpolarized.
So the signal for wakefulness is not transmitted.
Now when we use barbiturates, they prolong the duration of the Cl-
channel opening by binding to GABA receptor.
PHARMACOLOGICAL ACTIONS
CNS
Barbiturates induce sedation and sleep depending on dose.
Hypnotic dose shortens the time taken to fall asleep and increases
sleep duration as well.
Sedative dose may produce drowsiness and reduction in anxiety.
Phenobarbitone has selective anti-epileptic action.
Euphoria may be experienced by addicts.
RESPIRATION
Barbiturates depress the respiratory centre of the brain.
Death in barbiturate poisoning is due to respiratory depression.
CVS
Hypnotic doses of barbiturates produce a slight decrease in blood
pressure and heart rate.
Toxic doses produce remarkable fall in blood pressure and direct
decrease in cardiac contractility.
SKELETAL MUSCLES
Barbiturates reduce muscle contraction by inhibiting excitability of
neuromuscular junction.
SMOOTH MUSCLES
Hypnotic dose reduces muscle contraction and bowel movement.
KIDNEY
Barbiturates reduce urine flow by increasing ADH (anti diuretic hormone) release.
ADME (OR PHARMACOKINETICS)
ABSORPTION: Given through oral route. Barbiturates are well absorbed
by the GIT.
DISTRIBUTION: They are widely distributed throughout the body. Highly
lipid soluble barbiturates have instantaneous entry while less lipid soluble
ones take longer time.
METABOLISM: They are metabolized in liver by oxidation.
EXCRETION: Barbiturates are excreted in urine.
ADVERSE EFFECTS
Ø Hangover, mental confusion and impaired mental
alertness.
Ø Hypersensitivity reactions.
Ø Drug addiction and withdrawal syndrome.
Ø Mostly suicidal (patients may commit suicide).
Ø Motor driving in the road is risky due to
mental confusion (road accidents may happen).
THERAPEUTIC USES
Ø Used as Sedative-hypnotics
Ø Used as CNS depressant
Ø Used to treat insomnia
Ø Used as anaesthetics
Ø Used to treat epilepsy
14.
DEFINE DIURETICS.
CLASSIFY IT. WRITE DOWN THE PHARMACOLOGICAL ACTION, ADVERSE EFFECT AND USE OF
FUROSEMIDE.
ANS:
A diuretic is any substance that increases production of urine. They
help kidneys release more sodium into urine. The sodium helps remove water from
blood , decreasing the amount of fluid flowing through veins and arteries.
This reduces blood pressure and edema.
Diuretics, most commonly act via sodium reabsorption in the nephron.
EDEMA: Edema is swelling caused by excess fluid trapped in body’s
tissues (hands, arms, feet, ankles, and legs).
CLASSIFICATION
1. HIGH EFFICACY
DIURETICS (INHIBITORS OF Na+-K+-2Cl- COTRANSPORT)
Sulphamoyl derivatives: Furosemide,
Bumetanide, Torasemide
2. MEDIUM EFFICACY
DIURETICS (INHIBITORS OF Na+-Cl- SYMPORT)
A. Thiazides:
Hydrochlorothiazide, Benzthiazide, Hydroflumethiazide, Clopamide.
B. Thiazide like:
Chlorthalidone, Metolazone, Xipamide, Indapamide.
3. WEAK DIURETICS
A. Carbonic anhydrase
inhibitor: Acetazolamide
B. Potassium sparing
diuretics
i.
Aldosterone antagonist: Spironolactone
ii.
Inhibitors of renal epithelial Na+ channel:
Triamterene, Amiloride
C. Osmotic diuretics: Mannitol, Isosorbie, Glycerol
FUROSEMIDE (FRUSEMIDE)
Furosemide is a loop diuretic (as it acts at
the ascending limb of loop of Henle) medication used to treat fluid build-up
inside the body.
It can be taken by an injection into the
vein or by oral route. When taken by oral route, it starts working within an
hour, while intravenously, it starts working within five minutes.
The diuretic response increases with
increasing dose that means up to 10 L of urine can be produced in a day.
MECHANISM OF ACTION OF FUROSEMIDE
Furosemide act by inhibiting the Na+
-K+ -2Cl- cotransport in the ascending limb of the loop
of Henle.
So it causes more sodium, chloride, and
potassium to stay in the urine, preventing sodium reabsorption from the tubular
fluid.
This leads to diuresis.
In the ascending limb, about 25-30% of
sodium and water are reabsorbed which means a very high dose of Furosemide can
cause tremendous diuresis that’s why furosemide is called ‘High Efficacy
Diuretics’.
ADVERSE EFFECTS
1. Hypotension can
occur.
2. Hypokalemia (low potassium
level) can develop.
3. Hyperuricemia
(excess uric acid in the blood).
4. Ototoxicity (toxic
to ear) can occur.
5. Allergic reactions
USES
1. Furosemide is used
to treat acute pulmonary edema.
2. It is also used to
treat cerebral edema.
3. Furosemide is used
to treat Hypertension.
4. Also used to treat
renal calcium stones.
5. It is used to treat
Hyperkalemia (high potassium level).