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Pharmacokinetics, Sometimes Described As What The Body Does To A
Pharmacokinetics, Sometimes Described As What The Body Does To A
The main processes involved in pharmacokinetics are absorption, distribution, and the two routes of
drug elimination, metabolism and excretion. Together they are sometimes known by the acronym
'ADME'
They are absorption, distribution, metabolism, and excretion. Each of these processes is
influenced by the route of administration and the functioning of body organs
The pharmacokinetic characteristics can be quantitatively expressed by its parameters, such
as the elimination rate constant (denoted as K), half-life (t 1/2), apparent volume of distribution (V d)
and total clearance rate (CL)
Knowledge of pharmacokinetic principles helps prescribers adjust dosage more accurately and
rapidly. Application of pharmacokinetic principles to individualize pharmacotherapy is termed
therapeutic drug monitoring.
Precautions
Interactions
Overdose
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Uses
Use this medication regularly to get the most benefit from it. To help you
remember, take it at the same time each day. Keep taking this medication
even if you feel well. Most people with high blood pressure do not feel sick.
Etacrynic acid or ethacrynic acid, trade name Edecrin, is a loop diuretic used to treat high blood
pressure and the swelling caused by diseases like congestive heart failure, liver failure, and kidney
failure.
osmotic diuretic is a type of diuretic that inhibits reabsorption of water and sodium. They are
pharmacologically inert substances that are given intravenously. They increase the osmolarity of
blood and renal filtrate. Two examples are mannitol and isosorbide.
Osmotic diuretics
glycerin (Glycerol)
Isosorbide.
Mannitol IV.
Urea.
Osmotic Diuretics (Examples: Mannitol, Glycerin, Isosorbide, Urea) Osmotic diuretics are
relatively inert substances; they do not directly interact with renal transport systems
They increase the osmolarity of blood and renal filtrate. Two examples are mannitol and
isosorbide. In the nephron, osmotic diuretics act at the portions of the nephron that are water-
permeable. Osmotic diuretics work by expanding extracellular fluid and plasma volume, therefore
increasing blood flow
2. Uricosuric (antigout agents). Classification, principles of action. Drugs used in acute gouty
attack.
general, uricosuric drugs act on the proximal tubules in the kidneys, where they interfere
with the absorption of uric acid from the kidney back into the blood. Several uricosurics
are known to act in vitro by blocking the function of a protein encoded by the
gene SLC22A12, also known as urate transporter 1 or URAT1. URAT1 is the central
mediator in the transport of uric acid from the kidney into the blood. In some persons
with loss-of-function mutations of URAT1, the uricosurics benzbromarone and losartan
had no effect, suggesting these drugs act on URAT1 in vivo.[1] Thus, uricosuric drugs may
be candidates for management in a personalized medicine model
Allopurinol is in a class of medications called xanthine oxidase inhibitors. It works by reducing the
production of uric acid in the body. High levels of uric acid may cause gout attacks or kidney stones.
Allopurinol is used to prevent gout attacks, not to treat them once they occur.
Uricosuric Agents
Uricosuric agents lower uric acid levels by inhibiting renal tubular reabsorption
of uric acid, thereby increasing net renal excretion of uric acid. These agents
increase the risk of renal stones, with about a 9-10% risk for probenecid. They
should not be started during an attack of acute gouty arthritis. The goal of
therapy is to lower serum uric acid to approximately 5-6 mg/dL without
causing renal stones.
Primary uricosurics. The primary uricosuric drugs include probenecid, benzbromarone and
sulfinpyrazone.
Secondary uricosurics. Drugs with other primary uses, that have known uricosuric properties,
include losartan, atorvastatin, and fenofibrate. ...
Pharmacology. ...
Antiuricosurics. ...
See also. ...
References. ...
External links.
Uricosurics are drugs that promote the excretion of uric acid and are used in patients who have gout
(high uric acid levels leading to uric acid crystal formation in joints).
Uricosuric drugs were the first agents used to control hyperuricemia in patients with
gout.1 Any drug that increases renal excretion of uric acid, independently of the
mechanism through which it exerts its effect, may be considered a uricosuric
drug. Salicylates were the first drugs to be used to correct hyperuricemia of gout, as
they showed a paradoxical effect on renal handling of uric acid: they reduce renal
excretion at low doses and increase renal excretion at high doses. 2
The concept that underlines the term “uricosuric” may be misleading, if one considers
that these drugs will exert an effect on the renal handling of urate that will induce what
could be considered a hyperuricosuric state. However, it may certainly occur in subjects
who show normal renal excretion of uric acid in the hyperuricemic state.
The most actual concept would be to consider uricosuric drugs as drugs to be used to
correct hyperuricemia derived from “inefficient renal excretion” (IRE) of uric acid, 3 lately
known as “underexcretion,” that conceptually means that renal excretion of uric acid is
not found to the amount expected based on serum urate concentration (SUR) levels
and glomerular filtration, that is to say to the filtered load.4 Thus, our clinical approach to
the use of uricosurics will be to recognize them as means to normalize renal excretion
of uric acid in patients with IRE of uric acid. 5
In this chapter, we will further discuss the concept, targets, and clinical assessment of
IRE; drugs that increase renal excretion of uric acid, either approved, not approved, or
in development; and clinical management of uricosuric therapy, including combination
of xanthine oxidase inhibitors (XOIs) and uricosurics.
contracting strips of human myometrium. In (A), strips were superfused with PSS
(pH7.4, 37°C) followed by high potassium (40 mM KCl) depolarization (KCl, black
bar). In (B), the effect of removing external calcium (0Ca, black bar) on inhibition of
Uterine Contractility
TERTTU KATILA, in Current Therapy in Equine Reproduction, 2007
PHYSIOLOGICAL BASIS OF MYOMETRIAL CONTRACTILITY
The myometrium consists of two layers of smooth muscle with a
vascular zone in between. The muscle fibers of the outer longitudinal
layer are arranged parallel and those of the inner circular layers
concentrically around the long axis of the uterus. The spindle-shaped,
membrane-bound muscle cells are arranged into bundles of 10 to 50
cells. Neighboring cells come in close apposition in certain specialized
regions of their plasma membranes forming cell-to-cell contacts, which
are termed gap junctions. They are modifications of the apposing
plasma membranes of the adjacent cells and couple them electrically
and metabolically. The gap is a narrow space of about 2 to 3 nm, and
it is composed of a few thousand channels. 1
activates phosphatidylinositol 4,5 bisphosphate-
specific phospholipase C (PIP -PLC). This reaction catalyzes the
2
Female Reproduction
Peyvand Amini, Sam Mesiano, in Encyclopedia of Reproduction
(Second Edition), 2018
The Myometrium
For most of pregnancy the myometrium is relaxed, quiescent and
compliant, and grows mainly by stretch-induced cellular hypertrophy of
myometrial cells to accommodate the growing conceptus. The initial
phase of parturition involves a phenotypic transformation whereby
myometrial cells gain the capacity to contract forcibly, rhythmically and
coordinately, and become more responsive to uterotonic hormones
(factors that directly induce uterine contraction) such as oxytocin (OT)
and prostaglandin-F (PGF ). This transformation involves increased
2α 2α
The prostaglandins are a group of lipids made at sites of tissue damage or infection that
are involved in dealing with injury and illness. They control processes such as inflammation,
blood flow, the formation of blood clots and the induction of labour
Unlike most hormones, which are produced by glands and transported in the bloodstream to act on
distant areas of the body, the prostaglandins are produced at the site where they are needed.
Prostaglandins are produced in nearly all cells and are part of the body’s way of dealing with injury
and illness.
Prostaglandins act as signals to control several different processes depending on the part of the
body in which they are made. Prostaglandins are made at sites of tissue damage or infection, where
they cause inflammation, pain and fever as part of the healing process. When a blood vessel is
injured, a prostaglandin called thromboxane stimulates the formation of a blood clot to try to heal the
damage; it also causes the muscle in the blood vessel wall to contract (causing the blood vessel to
narrow) to try to prevent blood loss. Another prostaglandin called prostacyclin has the opposite effect
to thromboxane, reducing blood clotting and removing any clots that are no longer needed; it also
causes the muscle in the blood vessel wall to relax, so that the vessel dilates. The opposing effects
that thromboxane and prostacyclin have on the width of blood vessels can control the amount of
blood flow and regulate response to injury and inflammation.
Prostaglandins are also involved in regulating the contraction and relaxation of the muscles in
the gut and the airways.
Prostaglandins are known to regulate the female reproductive system, and are involved in the
control of ovulation, the menstrual cycle and the induction of labour. Indeed, manufactured forms of
prostaglandins - most commonly prostaglandin E2 - can be used to induce (kick-start) labour.
Beta-sympathomimetics
Action
Relaxation of the smooth muscle fibres by stimulating the beta receptors present on the cell membrane.
Examples:
Ritodrine (Yutopar):
Dosage: 50 mg of ritodrine in 500 ml of 5% glucose solution. Start by 10 drops per minute and increase by 5 drops
every 10 minutes until uterine contractions cease.
The infusion should be continued for 12-48 hours after cessation of contractions.
The treatment is then maintained by oral therapy as one tablet (10 mg) every 8 hours after meal to reduce
its side effects.
Maternal pulse and blood pressure as well as foetal heart rate should be monitored during treatment to
control the dose.
Side effects
Maternal:
o Tachycardia,
o hypotension (relaxation of the smooth muscle fibres in the blood vessels wall),
o flushing,
o sweating
o nausea,
o vomiting,
o headache,
o anxiety,
o tremors,
o hyperglycaemia,
o hypokalaemia,
o acidosis and
o pulmonary oedema.
Foetal:
o Tachycardia,
o arrhythmia,
o loss of beat-to-beat variation,
o neonatal hypotension and hypoglycaemia.
Contraindications
Heart disease.
Hypertension or hypotension.
Hyperthyroidism.
Antepartum haemorrhage (dilatation of the uterine arteries may increase the bleeding).
Diabetes.
Terbutaline,
Isoxuprine (Duvadilan - vasoxiprine) 20 mg 3-4 times daily.
Salbutamol.
Calcium Antagonists
Action: Antagonise the action of calcium within the myometrial cells so reduce its contractility.
Magnesium Sulphate
Action: The intracellular calcium is displaced by magnesium ion leading to inhibition of the uterine activity.
Dosage: The initial dose is 40 cc of 10% solution given slowly IV. The subsequent doses depend upon the response
and the development of MgSO4 toxicity so reflexes and respiratory rate should be observed.
Dosage: e.g. indomethacin 100 mg suppository initially, followed by 25 mg orally every 6 hours for up to 24 hours
after contractions ceased.
Ethyl Alcohol
Action
Dosage
It is given IV and the dose is adjusted to maintain blood alcohol level of 0.9-1.6 mg/litre.
Side effects
II. Write out a prescription and indicate the mechanism of action of the following
drugs:
1. Furosemide in ampoules:
Dt dn 10 in amp
2. Verospiron in tablets:
Ds do 1 tab bid
4. Sulfinpyrazone in tablets:
Rx : Sol sulfinpyrazone 0.1g
Ds po 1tab bid
5. Oxytocin in ampoules:
Rx : Sol oxytocin 1ml sol
Dt dn 10 in amp