Alcoholism's Impact on Liver Function

This assignment delves into the detrimental effects of excessive alcohol consumption on the liver. It examines liver function tests and coagulation profiles to demonstrate impaired liver function. The analysis also covers complications such as portal hypertension and ascites, outlining multidisciplinary management approaches involving medications to address blood pressure issues.

INTRODUCTION
Increase in alcohol consumption by chunk of population is considered be the major
concern in present scenario. The medical science has proved from time-to-time that alcohol has
range of negative impacts on human body. The report proposed herewith emphasizes on
analyzing various negative impacts of alcohol consumption. It throws light on manner in which
alcohol destroys organ’s capacity to control mechanism of human body.
ALCOHOLIC CIRRHOSIS EVALUATION
Use of alcohol leads to progressive damage of the liver to a point where cirrhosis occurs.
The liver has an innate ability to regenerate after an injury. However, continuous alcohol
drinking does not offer the liver an opportunity to heal.
Liver cirrhosis develops in heavy drinkers who drink more than 230 g of alcohol per day
(Galvani, 2012 p. 3). Apart from the drinking patterns, there seem to be other factors responsible
for an individual developing liver disease since not all people who drink heavily are affected.
Women require approximately half the alcohol percentage for susceptible men to develop the
same condition.
Alcohol is readily absorbed beginning from the stomach to the small intestine. Ethanol
cannot be stored in the body, and the degradation process begins in the gastric mucosa. On
reaching the liver, alcohol is acted upon by the liver enzymes, alcohol dehydrogenase (ADH) and
the cytochrome P-450 enzymes. The microsomal enzyme oxidation system (MEOS) also acts on
the substance in chronic alcoholism. ADH converts alcohol into acetaldehyde which is then
oxidized by acetaldehyde dehydrogenase (ALDH) to form acetate. In the process, hydrogen is
formed, and it serves to convert nicotinamide adenine dinucleotide (NAD) to NADH hence

increasing the liver’s redox potential. Fatty acid oxidation, as well as gluconeogenesis, is
inhibited, and the result is fat accumulation in the hepatocytes.
The export of fat to the rest of the body is hampered due to a reduction in the synthesis of
lipoproteins and hepatic fatty oxidation. The decreased export of fat leads to an increase in the
influx of fat in the liver as a result of peripheral lipolysis and synthesis of triglycerides. Alcohol
effects in the gut include changes in permeability and increase in absorption of bacterial
endotoxins. The Kupfer cells produce free radicals increasing the oxidative stress in the liver.
The under nutrition related to alcoholism leads to a reduced antioxidant action of glutathione,
vitamins A and E in the body. The body cells bind to acetaldehyde to form new antigens and
inflammatory response ensues. The white cells release inflammatory cytokines and interleukins
to deal with the antigens.
High blood pressure in the liver venous system is caused by cirrhosis (Runyon, 2013 p.
1651). The normal blood flow through the liver parenchyma is slowed, and the pressure in the
veins is increased. Portal hypertension causes fluid to accumulate in the extremities and the
abdomen. The reason is that the liver cirrhosis leads to the inability of the liver to manufacture
proteins that maintain the oncotic pressure such as albumin. Splenic damage due to cirrhosis
leads to a reduced white blood cells, platelets, and red cells due to sequestration and the patients
become easily fatigued. Malnutrition due to cirrhosis also leads to the inability of the body to
accumulate nutrients and hence the easy fatigability. The liver is damaged leading to
hepatomegaly with a firm, sharp edge. Portal hypertension leads to hypoxemia and
intrapulmonary arteriovenous shunting, and the patient becomes tired on little exertion. Liver
cirrhosis leads to a raised blood pressure that may push a patient towards hypertension. The
endotoxic damage from the gut bacteria leads to the gastrointestinal symptoms of anorexia,

indigestion, constipation, and diarrhea (Bajaj et al., 2014 p. 943). Liver cirrhosis also leads to
biliary malfunction and hence reduced digestive functions of the bile duct. This in turn leads to
an increased transit time in the gut and constipation.
The glucose levels are within range, and this is an indication that the patient’s status is
not progressing towards diabetes. However, more tests on glucose are required before a
conclusion is made. Alcohol interferes with the production of leukocytes in the bone marrow.
The leukocyte levels of Mr. Chris are within limits for his age group. The hematocrit level of 38
% however, raises the alarm because it is slightly reduced. The patient is, therefore, anemic, a
factor that is associated with alcoholism. The anemia results from both nutritional deficiency and
infections that an alcoholic is predisposed. The process of iron absorption is interfered with by
alcohol, and resulting condition is iron deficiency anemia. The iron loss can also come from the
bleeding in gut and esophageal varices. Folic and other vitamin deficiencies due to excessive
alcohol consumption can also cause anemia in the alcoholics (Ballard, 1997 p. 43).
The blood-clotting mechanisms of body are affected by excessive alcohol consumption
(Trevejo-Nunez, 2015 p. 177). The platelets secrete clotting factors and proteins responsible for
hemostasis. The effect of alcohol can be thrombocytopenia or low levels of platelets,
thrombocytopathy (impaired function of platelets and inhibition of fibrinolysis hence formation
of thrombi). The platelet levels are way below normal range for Mr. Chris. Some studies show
that alcohol may be leading cause of extremely low platelet count in individuals apart from those
who are immune compromised. Patients who have low platelets are at risk of bleeding disorders
that are difficult to control. Thrombocytopenia is self-limiting, and it takes only a week to restore
normal platelet counts if the patient abstains from drinking alcohol.

While activated coagulation time is within normal range, the prothrombin time and
partial thromboplastin time are way above limits. Both intrinsic and extrinsic clotting pathways
of patient are affected. The patient loses too much blood if a blood vessel is exposed when
compared to a normal individual whose clotting factors are functioning. The loss of blood can be
useful in explaining anemia as shown by reduced hematocrit. Wounds and ulcers in patient will
take longer to heal as compared to a person with normal coagulation profile.
Bilirubin is a byproduct of blood, and it is formed in t liver for excretion through the bile.
The total bilirubin levels are very high. The direct bilirubin levels are similarly elevated. The
subtraction of direct bilirubin from total bilirubin gives indirect bilirubin levels, and they are also
much elevated. The liver damage is extensive as shown by raised levels of bilirubin in the blood.
The reason is that pathway for elimination of excess bilirubin is blocked by swelling liver.
The liver function tests ALP, AST, and ALT, are all raised (Hoekstra, 2013 p. 28). The
biomarkers of functioning of liver have been raised to indicate that liver cells have been
damaged. Serum albumin and globins are raised in liver disease as seen in laboratory results of
the patient. The blood urea nitrates, as well as serum creatinine, are also raised when cells in
body are damaged as in oxidative damage caused by alcoholism. The serum sodium and calcium
are lowered in excessive alcohol intake. The nerve conduction and impulses may be hindered in
the patient if the levels of electrolytes are not maintained.
The initial dose of IV 0.9 % NaCl 500 ml with B- Dose 2 ml and 15 mg folate injection
was required for volume expansion and correction of micronutrient deficiency. NaCl is a source
of fluid and electrolytes that are usually depleted in alcoholic patients. The B-Dose 2 ml injection
is loaded together with the NaCl and contains an array of vitamins including thiamine, riboflavin,
nicotinamide, pyridoxine, cyanocobalamin, and dexpanthenol. Together with the folic acid, the

B-Dose would replenish the body’s stores of vitamins and assist in quick recovery of the patient
through abating the anemia. Folic acid and cobalamin are used in the DNA synthesis of the body
cells and especially in the bone marrow where erythropoiesis takes place. Gut symptoms and
ulcerations are relieved by the increased oxygenation and perfusion due to increased hemoglobin
and other blood components that lead to coagulation. Thiamine prevents beriberi while niacin
protects the patient from pellagra. The glucose is energy providing and more is needed in people
with liver cirrhosis because of the increased metabolic demands.The nervous system and the
brain functioning is enhanced by thiamine intake (Isenberg-Grseda et al., 2014 p. 4).
Spironolactone is a K sparing diuretic that serves to relieve the patient from the
symptoms of fluid retention. Mr. Chris has had two surgical interventions in the form of
paracenteses to relieve excessive fluid accumulation in the abdomen (Runyon, 2004 p. 48). The
condition needs an additional measure in the form of a diuretic that will act to reduce the total
body water. The drug will counter the effects of aldosterone, a natural regulator of salt and water
in the body. With continuous alcohol intake, the potassium levels in the body may reduce and
cause nerve disturbances. The potassium-sparing diuretic therefore helps to maintain appropriate
levels of the electrolyte in the system. In people who cannot handle the water in their systems, an
infusion of normal saline in large volumes may lead to a congestive cardiac failure.
Spironolactone, therefore, prevents the congestion in the heart by releasing the excess body
water through urine. Hypertension can be managed effectively by use of Spironolactone as the
excess pressure in the blood is relieved by excretion of water in the kidneys.
Hydrochlorothiazide lowers the blood pressure significantly. Just like Spironolactone, the
drug acts by making the patient lose more water in the urine. The diuretic effect allows the body
to lose more unwanted salts and water (Ginès et al., 2004 p. 1651). With reduced fluid and water,

edema is relieved and the pulmonary symptom of shortness of breath due to raised and restricted
diaphragm is solved. The drug is a prophylactic against stroke and cerebrovascular accidents as
well as heart and kidney diseases. A patient with alcohol problems needs to maintain their blood
pressure within the normal limits since the adaptability of their bodies is reduced in the case of
an unfavorable event.
Pheniramine maleate also goes by the name Avil and is a drug classified as an
antihistamine. Avil drug manages allergic conditions like a runny nose, hay fever, and pruritic
skin rashes. The pathophysiology of the liver cirrhosis reveals that the liver is highly inflamed
and therefore there is the need to reduce the inflammatory response of histamine. In liver disease,
the hepatocytes are damaged continually, and their function is reduced. The drug relieves the
inflammatory response and allows the liver cells to heal on their own.
Mylanta is an antacid drug, is very effective in treating heartburn and indigestion which
is among the presenting complaints in the patient with liver disease. Mylanta works on the excess
acid in the stomach so as to reduce its actions in the subsequent parts of the GIT that require a
basic medium for digestion (Borody, 2015 p. 1). By alkanizing parts of the small intestines, the
drug allows digestion and absorption to continue and hence relieving constipation.
The most common adverse event of NaCl infusion is fever, injection site tissue swelling,
redness, and fluid overload in overzealous IV doses. Hydrochlorothiazide side effects are
stomach upset, headaches and dizziness (Sukalo et al., 2016 p. 299). Few people have reported
the side effects, and even so, the benefits of taking the drug have always outweighed the risks.
Other people report dehydration with vision disturbances, muscle cramps, and palpitations with
dry mucous membranes. NSAIDS interacts with the drug to cause worsening edema and blood

pressure. The thyroid studies are affected by use of hydrochlorothiazide and false results may be
reported.
Abdominal cramps and other GIT disturbances have been associated with
Spironolactone. The drug can also lead to bleeding tendencies, especially in the gums, with
melena and blood in urine also reported (Strunk & Mayer, 2013 p. 311). In women, breast pain is
a common complaint when using the drug. Other people have experienced chills, chest pains,
and clay-colored stools, cloudy urine, and other urinary abnormalities. The central nervous
systems side effects are confusion, convulsions, headache, and trembling. Hyperkalemia can
result due to interactions of Spironolactone and angiotensin converting enzyme inhibitors,
heparin or aldosterone blockers. Alcohol and barbiturates cause orthostatic hypotension when
used together with the drug. Corticosteroid use leads to hypokalemia and NSAIDS reduce the
actions of the potassium-sparing diuretic.
Avil has been known to cause drowsiness and somnolence because of its sedative actions.
People who operate machinery or drive vehicles can be at a risk of serious accidents if they
perform the actions while of the drug. Nervousness, tinnitus, nausea, and vomiting are common
in people who take Avil. The drug may cause difficulty in micturition, irritability and lack of
coordination. Changes in moods and behavior and hallucinatory tendencies have been reported in
people using the drug. Hypersensitivity can be caused by the drug, and the patient complains of
hives, fainting episodes, jaundice and swelling of parts of the body. Drug interactions include
those of atropine and MAO inhibitors where they interfere with the actions of each other
(Katzung, 2011 p. 279).
Mylanta causes nausea, constipation, headaches, and diarrhea while the drug interferes
with the absorption of other medications (Zajac et al., 2013 p. 82). The B-Dose injection may

cause skin allergies, bruising, headaches, and fatigue. The vitamin supplements interact with
hydralazine, L-dopa and antiepileptic drugs causing interference in the absorption and plasma
levels of these drugs.
CONCLUSION
In summary, excessive consumption of alcohol over a long period leads to grievous
damage to the liver cells. The functions of the liver are decreased as shown by the liver function
tests as well as the coagulation profile of the patient which become deranged. The management
of the patient is multidisciplinary and requires the use of drugs that lower the blood pressure to
help deal with the portal overload.

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