Kelly's Case Study

KELLY’S CASE STUDY.
Introduction.
This is a descriptive essay. It will describe the case of Kelly, a 32-year-old pregnant female.
She is in her second trimester. She has a past medical history of severe viral hepatitis. She got
this when she spent 6 months overseas while at the age of 22 years old. This resulted in
permanent liver dysfunction. She also has a history of hyperemesis and sciatica in her previous
pregnancy. Sciatica continued even after her pregnancy. She has now ceased her medication for
the sciatica pain and the sciatica pain has increased significantly leading to discomfort. Kelly has
also been suffering from hyperemesis again since she was 8 weeks pregnant and it is increasing
in intensity. Kelly has had hospital admission for rehydration and she is now on paracetamol to
manage the sciatic pain condition. She is also on metoclopramide, a drug in the pro kinetic class
is clinically indicated to manage her hyperemesis (Giudicessi et al. 2018). though she is finding
it ineffective and she is thinking of starting taking Ondansetron to manage the same. The
persistent sciatic pain and hyperemesis is frustrating her and gives her a challenge of caring for
her 3-year-old child. The essay will, therefore, describe the pathophysiological concepts of the
conditions, a description of pharmacokinetics and pharmacodynamics of some of the drugs
administered. Focusing on how they work and their interactions with the human body. The
descriptive essay will then end with a conclusion outlining all the discussion throughout the
essay.
Question 1
Sciatica is a pain that radiates along the sciatic nerve, running downwards along one leg or both
legs from the lower back (During, 2015). Sciatica normally happens when the sciatic nerve (the
largest nerve) is compressed. Sciatica nerve starts at the lower back and runs down the buttocks
then branches down the back of the legs to the ankles and feet. When this nerve is compressed it
leads to pain that is sharp, tingling and shooting. Many cases of sciatica occur as a result of
spinal disc bulge or herniation. The weakening of the annulus fibrosus, an outer nucleus of the
intervertebral spinal disc makes it at a high risk of becoming less rigid and becomes more likely
to tear. Tear in the annulus fibrosus causes extrusion of the nucleus pulposus pressing against the
spinal nerves causing pain. When the tearing happens at the spine near the sciatic nerve then
compression of the sciatic nerve causes sciatica.

Sciatica in pregnancy occurs commonly at the second or the third trimester (Proisy et al., 2014,
pp.828-838). The increased sciatica pain in Kelly during her second trimester is due to the
following; Muscle tension and increased pelvic pressure. The increased pelvic pressure can be
due to increasing baby weight, increasing uterus, increased fluid retention an in joints and pelvic
bone pain due to the increased baby's weight.
The increasing baby's weight adds pressure on the sciatic nerve either directly or on the hip joint
and the pelvic bone. During pregnancy, there is a possibility of Kelly retaining excess fluid
which can at a time put pressure on an exposed sciatic nerve. The growing uterus also increases
the pressure exerted on the sciatic nerve. Apart from increased pressure, the second reason that
has caused Kelly's sciatica is muscle tension. The increased pressure on the pelvic region can
lead to the manifestation of the sciatic symptoms. In her pregnancy, Kelly produces a hormone
called relaxin. This hormone is more potent in the pelvic area causing stretching and loosening of
ligaments (Sailaja, 2015) ,
Question 2.
Hepatitis is the inflammation of the liver which results in pain redness and swelling. It is caused
by a virus, and can either be acute (lasting at a less duration of time) or it can be long-lasting,
lasting more than the 6 months. Kelly got long-lasting hepatitis which resulted in permanent liver
failure. Kelly is on medication to manage her condition s and one of the drugs she is prescribed
with is paracetamol to manage her sciatic pain. Paracetamol as a drug can be administered orally
or rectal. When administered orally it is well absorbed in the gastrointestinal tract and its oral
bioavailability is drug dependent. Increased in dosage reduces the hepatic first-pass effect (Imani
et al., 2014), this is due to the overwhelming effect of the enzymatic capacity and therefore its
bioavailability increases. Thus, the half-life for toxic doses increases from 2-4 hours to 4-8
hours. Paracetamol is metabolized in the liver, most of its metabolites are conjugated and the
remaining small amount is hydroxylated to N-acetyl-benzoquinone imine. It reacts with the
sulfhydryl groups in the glutathione. Overdose leads to depletion of the glutathione and thus it
binds to the hepatocytes and renal tubular cells leading to hepatic and renal failure. (Lancaster,
Hiatt & Zarrinpar, 2015). paracetamol is therefore eliminated mostly by hepatic metabolism, and
now that Kelly’s liver is dysfunctional, she has a considerably longer elimination half-life. On
the other hand, Metoclopramide also undergoes first-pass hepatic metabolism. It is partially

metabolized by cytochrome P450 system. Its oral bioavailability ranges from 30%-100%.
Impaired clearance of the drug is seen in marked hepatic impairment leading to increased
adverse effects due to the accumulation of the drug as a result of lowered clearance. For a patient
with the normal renal system but an impaired hepatic system, the dose can be safe but should be
reduced to half.
Question 3
Kelly has got more than one condition affecting her and they are managed medically with the use
of different types of drugs which treat the different conditions. One of the conditions is the
hyperemesis and the current antiemetic medication that Kelly takes is metoclopramide. Being an
anti-emetic drug, it is therefore clinically indicated to manage her hyperemesis condition. Apart
from reducing nausea and vomiting, metoclopramide can also be clinically indicated to delay
stomach emptying and to patients with gastroesophageal reflux disease. The mechanism of
action of metoclopramide is due to its antagonist activity at D2 receptors (Rojas et al., 2014,
pp.26-37). D2 receptors are found at the chemoreceptor trigger zone. Metoclopramide binds at
these receptors and at higher doses it can bind to serotonin receptors (5HT3) as well to cause
anti-emetic effect as well. Metoclopramide has a gastroprokinetic effect that is mediated by
muscarinic activity, serotonin agonist activity, and dopamine receptor agonist activities.
Metoclopramide also promotes gut motility and thus increasing gut emptying. Increased gut
emptying reduces the rate at which someone can experience nausea and vomiting.
Metoclopramide does so in three mechanisms; it inhibits both the presynaptic and postsynaptic
D2 receptors, it also stimulates the presynaptic excitatory 5-HT 4 receptors and lastly is the
antagonism of presynaptic inhibition of muscarinic receptors. However, the prokinetic properties
of metoclopramide are limited to the proximal gut.
Question 4
The mechanism of action of her current medication, metoclopramide is binding antagonistically
at the dopamine receptors or the serotonin receptors. Dopamine type receptors are found at the
chemoreceptor trigger zone (Moon, 2014, p 164). The chemoreceptor trigger zone is an area of
the medulla which receives inputs and communicates with other structures of the vomiting
center. The other neurotransmitters that are in the chemoreceptor trigger zone that takes part in
controlling nausea and vomiting too include acetylcholine, histamine, and substance P. The