ALCOHOLIC LIVER DISEASE

INTRODUCTIONDefinition and causesLiver disease related to alcohol consumption fits into one of three categoriesfatty liver, alcoholic hepatitis, or cirrhosis. Fatty liver, which occurs after acute alcohol ingestion, is generally reversible with abstinence and is not believed to predispose to any chronic form of liver disease if abstinence or moderation is maintained. Alcoholic hepatitis is an acute form of alcohol-induced liver injury that occurs with the consumption of a large quantity of alcohol over a prolonged period of time; it encompasses a spectrum of severity ranging from asymptomatic derangement of biochemistries to fulminant liver failure and death. Cirrhosis involves replacement of the normal hepatic parenchyma with extensive thick bands of fibrous tissue and regenerative nodules, which results in the clinical manifestations of portal hypertension and liver failure.Table 1: Forms of Alcoholic Liver DiseaseParameterFatty LiverAlcoholic HepatitisCirrhosis

Histologic specificity for alcoholic causeNoYesNo

PrognosisExcellentVariableGuarded

ReversibleYesVariableGenerally, no

Prevalence and risk factorsThe prevalence of alcoholic liver disease is influenced by many factors, including genetic factors (e.g., predilection to alcohol abuse, gender) and environmental factors (e.g., availability of alcohol, social acceptability of alcohol use, concomitant hepatotoxic insults), and is therefore difficult to define. In general, however, the risk of liver disease increases with the quantity and duration of alcohol intake. Although necessary, excessive alcohol use is not sufficient to promote alcoholic liver disease. Only one in five heavy drinkers will develop alcoholic hepatitis, and one in four will develop cirrhosis.Different alcoholic beverages contain varying quantities of alcohol . Although fatty liver is a universal finding among heavy drinkers, up to 40% of those with modest alcohol intake (up to 10 g per day) will also exhibit fatty changes. Based on an autopsy series of men, a threshold daily alcohol intake of 40 g was necessary to produce pathologic changes of alcoholic hepatitis. Consumption of more than 80 g per day was associated with an increase in the severity of alcoholic hepatitis, but not in the overall prevalence. There is a clear dose-dependent relation between alcohol intake and the incidence of alcoholic cirrhosis. A daily intake of more than 60 g of alcohol in men and 20 g in women significantly increases the risk of cirrhosis. In addition, steady daily drinking, as compared with binge drinking, appears to be more harmful.Table 2: Alcohol Content of Some Common BeveragesDrinkAmount (oz)Absolute Alcohol (g)

Beer1212

Wine512

Liquor (80 proof)1.512

Pathophysiology and natural historyThe liver and, to a lesser extent, the gastrointestinal tract, are the main sites of alcohol metabolism. Within the liver, there are two main pathways of alcohol metabolism, alcohol dehydrogenase and cytochrome P-450 2E1. Alcohol dehydrogenase is a hepatocyte cytosolic enzyme that converts alcohol to acetaldehyde. Acetaldehyde subsequently is metabolized to acetate via the mitochondrial enzyme, acetaldehyde dehydrogenase. Cytochrome P-450 2E1 also converts alcohol to acetaldehyde.Liver damage occurs through several interrelated pathways. Alcohol dehydrogenase and acetaldehyde dehydrogenase cause the reduction of nicotinamide adenine dinucleotide (NAD) to NADH (reduced form of NAD). The altered ratio of NAD/NADH promotes fatty liver through the inhibition of gluconeogenesis and fatty acid oxidation. Cytochrome P-450 2E1, which is upregulated in chronic alcohol use, generates free radicals through the oxidation of nicotinamide adenine dinucleotide phosphate (reduced; NADPH) to NADP. Chronic alcohol exposure also activates hepatic macrophages, which then produce tumor necrosis factor a (TNF-). TNF- induces mitochondria to increase the production of reactive oxygen species. This oxidative stress promotes hepatocyte necrosis and apoptosis, which is exaggerated in the alcoholic individual who is deficient in antioxidants such as glutathione and vitamin E. Free radicals initiate lipid peroxidation, which causes inflammation and fibrosis. Inflammation is also incited by acetaldehyde that, when bound covalently to cellular proteins, forms adducts that are antigenic. Histologically, the earliest changes in alcoholic hepatitis are located predominantly around the central vein. Alcohol is known to cause an exaggerated gradient of hypoxia from the portal vein to the central vein, suggesting that the hypoxia induced by chronic alcohol use may contribute to hepatic damage.With abstinence, morphologic changes of the fatty liver usually revert to normal. Although the short-term prognosis in patients with alcoholic steatosis is excellent, with longer follow-up it has been found that cirrhosis develops more commonly in alcohol abusers with fatty liver changes than in those with normal liver histology. Morphologic features predictive of progression to fibrosis, cirrhosis, or both include severe steatosis, giant mitochondria, and the presence of mixed macrovesicular-microvesicular steatosis.Historically,the 30-day mortality rate in patients with alcoholic hepatitis ranges from 0% to 50%. Clinical and laboratory features are powerful prognostic indicators for short-term mortality. Hepatic encephalopathy, derangement in renal function, hyperbilirubinemia, and prolonged prothrombin time are seen more frequently in patients who succumb to their illness than in those who survive. Both the discriminant function and the model for end-stage liver disease (MELD) score can be used to predict short-term mortality in patients with alcoholic hepatitis. The MELD score is calculated based on a patient's prothrombin time, serum creatinine, and bilirubin; a calculator can be found on the United Network for Organ Sharing website. Long-term survival in patients with alcoholic hepatitis who discontinue alcohol is significantly better than in those who continue to drink, although it remains considerably below that of an age-matched population. Three-year survival approaches 90% in abstainers, whereas it is less than 70% in active drinkers.Cirrhosis has historically been considered to be an irreversible outcome of severe and prolonged liver damage. However, studies involving patients with liver disease from many distinct causes have shown convincingly that fibrosis and cirrhosis may actually have a component of reversibility. For those patients with decompensated alcoholic cirrhosis who undergo transplantation, survival is comparable with that of patients with other causes of liver disease (approximately a 70% 5-year patient survival rate).Signs and symptomsPatients with fatty liver are typically either asymptomatic or present with nonspecific symptoms that do not suggest acute liver disease. Supporting features on physical examination include an enlarged and smooth, but rarely tender, liver. In the absence of a super-imposed hepatic process, stigmata of chronic liver disease such as spider angiomas, ascites, or asterixis should be absent.Alcoholic hepatitis is a syndrome with a spectrum of severity, and therefore manifesting symptoms vary. Symptoms may be nonspecific and mild and include anorexia and weight loss, abdominal pain and distention, or nausea and vomiting. Alternatively, more severe and specific symptoms may include encephalopathy and hepatic failure. Physical findings include hepatomegaly, jaundice, ascites, spider angiomas, fever, and encephalopathy. When alcoholic hepatitis is more severe, the differential diagnosis includes autoimmune hepatitis, acute viral hepatitis, acute Budd-Chiari syndrome, severe drug-induced liver injury, and an acute manifestation of Wilson's disease.Established alcoholic cirrhosis may manifest with decompensation without a preceding history of fatty liver, alcoholic hepatitis, or any other alcohol-related diagnosis. Alternatively, alcoholic cirrhosis may be diagnosed concurrently with acute alcoholic hepatitis. The symptoms and signs of alcoholic cirrhosis do not help differentiate it from other causes of cirrhosis. Patients may present with jaundice, pruritus, abnormal laboratory findings (e.g., thrombocytopenia, hypoalbuminemia, coagulopathy), or complications of portal hypertension, such as variceal bleeding, ascites, or hepatic encephalopathy.Fatty liver is usually diagnosed in the asymptomatic patient who is undergoing evaluation for abnormal liver function; results include usually mildly elevated aminotransferase levels lower than twice the upper limit of normal. Laboratory tests are not diagnostic of fatty liver. Characteristic ultrasonographic findings include a hyperechoic liver with or without hepatomegaly. Liver biopsy is rarely needed to diagnose fatty liver in the appropriate clinical setting, but may be useful in excluding steatohepatitis or fibrosis. Typical histologic findings of fatty liver include fat accumulation in hepatocytes that is often macrovesicular, but may occasionally be microvesicular The centrilobular region of the hepatic acinus is most commonly affected. In severe fatty liver, however, fat is distributed throughout the acinus. Fatty liver is not specific to alcohol ingestion; it is associated with obesity, insulin resistance, hyperlipidemia, malnutrition, and various medications. Attribution of fatty liver to alcohol use therefore requires a detailed and accurate patient history.The diagnosis of alcoholic hepatitis is based on a thorough history, physical examination, and review of laboratory tests. Characteristically, the aspartate aminotransferasetoalanine aminotransferase ratio (AST/ALT) is approximately 2:1, and the absolute value of the aminotransferase levels does not exceed 300 U/L unless a superimposed hepatic insult exists, such as acetaminophen toxicity. Other common and nonspecific laboratory abnormalities include anemia and leukocytosis. Liver biopsy is occasionally necessary to secure the diagnosis. The classic histologic features of alcoholic hepatitis include inflammation and necrosis, which are most prominent in the centrilobular region of the hepatic acinus. Hepatocytes are classically ballooned, which causes compression of the sinusoid and reversible portal hypertension. The inflammatory cell infiltrate, located primarily in the sinusoids and close to necrotic hepatocytes, consists of polymorphonuclear cells and mononuclear cells. In addition to inflammation and necrosis, many patients with alcoholic hepatitis will have fatty infiltration and Mallory bodies, which are intracellular perinuclear aggregations of intermediate filaments that are eosinophilic on hematoxylin-eosin staining. Neither fatty infiltration nor Mallory bodies are specific for alcoholic hepatitis or necessary for the diagnosis.The diagnosis of alcoholic cirrhosis rests on finding the classic signs and symptoms of end-stage liver disease in a patient with a history of significant alcohol intake. Patients tend to underreport their alcohol consumption, and discussions with family members and close friends may provide a more accurate estimation of alcohol intake. Patients may present with any or all complications of portal hypertension, including ascites, variceal bleeding, and hepatic encephalopathy. The histology of end-stage alcoholic cirrhosis, in the absence of acute alcoholic hepatitis, resembles that of advanced liver disease from many other causes, without any distinct pathologic findings

The overall clinical diagnosis of alcoholic liver disease, using a combination of physical findings, laboratory values, and clinical acumen, is very accurate. However, liver biopsy can be justified in select cases, especially when the diagnosis is in question. In addition to confirming the diagnosis, liver biopsy is also useful for ruling out other unsuspected causes of liver disease, better characterizing the extent of the damage, providing prognosis, and guiding therapeutic decision making. As emphasized in the recent practice guidelines for alcoholic liver disease from the American College of Gastroenterology), liver biopsy is a relatively safe procedure, with morbidity lower than 0.6% and mortality lower than 0.03%. With a typical presentation, liver biopsy is not mandatory to diagnose alcoholic liver disease.

DEMOGRAPHIC DATAPatients name: Patient GirlushAddress: N/ASex: FemaleAge: 48 y.o.Civil Status: MarriedReligion: Roman CatholicNationality: FilipinoDate of admission: March 6, 2010Chief complaint: Vomiting and feverFinal Diagnosis: Alcoholic liver disease secondary to AGE with some dehydrationNURSING HISTORYPRESENT HEALTH HISTORYMarch 2, 2010 that was Monday at around 8:00 in the morning when patient Girlush experienced episode of nausea and vomiting until it persist up to five days and it was already accompanied by a high degree of fever thats why her husband decided to brought her at the hospital.PAST HEALTH HISTORYAccording to the client she completed her immunization during childhood. She usually experienced cough, colds and fever and her husband usually brought a solmux for her cough, neozep for her colds, and paracetamol for her fever.

At the age of 43 according to the client she was hospitalized at Cagayan Valley Medical Hospital due to of convulsion.

FAMILY HISTORYAccording to the S.O. there is no hereditary disease can be attributed from the patients fathers side, but the patients mother had a family health history of hypertension, Heart disease, and Diabetes mellitus.SOCIAL HISTORYAccording to the patients son his mother usually watches T.V and sometimes she went to her neighbors with same age just to have mingled with them and sometimes she played with her grandson and granddaughter.

GORDONS FUNCTIONAL HEALTH PATTERN1. Health perception and health management

>Before hospitalizationHealth for her is important but she has no sufficient knowledge on how to take care of herself.>After hospitalizationThe S.O. now views how important health management is.

2. Nutritional-metabolic pattern

>Before hospitalizationThe client takes three meals a day which compose commonly fish, vegetable, and meat and she only consume one cup of rice every meal. She drinks 3 to 4 glasses of water every day, 1 bottle of soft drink particularly coke, sprite, pop, royal or sparkle every week, 3-4 bottles of liquor particularly red horse every week, 2-3 glasses of juices particularly eight oclock every week and a cup of coffee a day.>During hospitalizationHer physician ordered her a BRAT diet and last March 10, 2010 the physician ordered her to temporarily not to take any foods for 1 hour in preparation for ultra sound. 3. Elimination pattern

>Before hospitalizationThe patient urinates three to five times a day ranging 4 glasses or 960ml and it is a light yellow in color and defecates once a day every morning with yellow color and in soft consistently.

>During hospitalizationThe patient is able to urinate 4 times a day ranging 2 and glasses or 600ml it is a light yellow in color and defecates once a day.

4. Activity exercise pattern>Before hospitalization The patient was able to perform activities such as bathing, toileting, dressing and tooth brushing 2 times a day and other self care activities. She did household chores in their house as her daily exercise during her vacant hours. She was able to watch television for about six hours.

>During Hospitalization The patient is able to perform self care activities without the assistance of her S.O.

5. Sleep rest pattern>Before hospitalization The client usually sleeps for about 8 hours every day from 11:00 in the evening to 7:00 in the morning and she doesnt have an afternoon nap.

>During hospitalization The client has an intermittent sleep, she begins to sleep at 9:00 in the evening and woke up due to the ward stimuli and then continue to sleep again. The patient has an afternoon nap at 3:00 in the afternoon.

6. Cognitive perceptual pattern

>Before hospitalizationShe can speak tagalong and Ilocano as her primary dialect. The patient can interact and express herself clearly and she doesnt have any hearing difficulties or visual problem.

>During hospitalizationThe patient can still follow instructions. She is still able to read and write letters and still able to express herself. 7. Self perception-self concept pattern

>Before hospitalizationAccording to the client she was loved by her husband and two children. Her two children were her inspiration and her and she wants a bright future for her grandson and granddaughter. >During hospitalizationAccording to the client she is still loved by her family and she stated that she at her age is still strong to do her routine activities.

8. Role relationship pattern

>Before hospitalizationAccording to the patient she was the only one who did household chore like; cooking, cleaning their house, fetch water and the like. She also takes her grandson and granddaughter a bath before going at her work and shower before sleeping.

>During hospitalizationAccording to the client she is unable to do household chores because of her condition and she is also unable in taking care her grandson and granddaughter.

9. Sexuality reproductive pattern

>Before hospitalizationAccording to the patient they did sexual activity with her husband and as the fruit of their love they are able to have two children.

>During hospitalizationAccording to the client she cannot express her love to her husband due to her condition.

10. Coping stress tolerance

>Before hospitalizationAccording to the client she manages her stress through bonding with her children during dinner time, playing with her grandson and granddaughter and watching TV for about six hours every day.

>During hospitalizationAccording to the patient she manages her stress through having a nap at around 3:00 in the afternoon.

11. Values and belief pattern>Before hospitalization She doesnt attend the Sunday mass but her faith to God is still on her.

>During hospitalization According to the patient she cannot attend the Sunday mass because of her situation but she is praying for her condition.

PHYSICAL ASSESSMENTGeneral appearance: weak looking, ecteric sclera, flabby soft abdomen, afebrile.Vital Signs:1. Temperature: 38.9C1. Respiratory Rate: 32cpm1. Pulse Rate: 90bpm1. Blood Pressure: 120/80mmhgBODY PARTSMETHOD USENORMAL FINDINGSABNORMAL FINDINGSANALYSIS

Head1. Hair

1. Scalp

1. Face

1. Skin>inspection

>inspection

>palpation

>inspection

>inspection>black hair, evenly distributed>no infection or infestation>rounded in shape>no mass and tenderness>no facial asymmetry>dark complexion

EYES1. Eyebrows

1. Eyelid

1. Eyelashes

1. Conjunctiva

1. Sclera

1. Eyeballs

1. Pupils

>inspection

>inspection

>inspection

>inspection

>inspection

>inspection

>inspection

.>inspection

>hair evenly distributed and equal in movement>upper lid covers, small portion of the iris and cornea; lower lid margin is just below the cornea and sclera>equally distributed with Black eyelashes and curled slightly outward>shiny, smooth and pink

>whitish w/o discoloration

>symmetrical

>black in color , equal in size, isometric 3-4 mm, round in shape and iris flat and round>reactive to light

>Ecteric

>Due to increased bile circulating in the blood

EARS1. Pinna

1. External canal>inspection

>palpation

>inspection>color same as facial skin; symmetrical>firm and not tender;Recoils after it is folded>dry skin; minimal cerumen and various shades of brown

NOSE

>inspection

>palpation>symmetric and straight

>not tender, no lesions

MOUTH1. Lips

1. Gum>Inspection

>Inspection>Moist and darker in color

>No bleeding and lesions

NECK1. Muscle

1. Lymph nodes>Inspection

>palpation>Muscles are equal in size; Head centered

SHOULDER

>inspection>palpation>symmetrical>no swelling

UPPER EXTRIEMITIES1. Skin

1. Nails

1. muscle and tone

>inspection

>palpation

>inspection

>palpation

>inspection

>dark complexion

>good skin turgor>convex curvature

>prompt return of pink or usual color

>equal size on both sides of the body

CHEST

>inspection

>palpation

>percussion

>auscultation>chest symmetric>no tenderness or masses>normal percussion sound

ABDOMEN

>inspection

>auscultation

>percussion

>palpation

>uniform color; flat abdomen

>audible bowel sounds>dullness specially in the liver and spleen

>no tenderness>Bloaty abdomen

>Thumpy sound

>Soft>Due to excessive peritoneal fluid

>Due to excessive fluid in the peritoneal cavity> Due to excessive fluid in the peritoneal cavity

LOWER EXTREMITIES

1. Skin

1. Toenails

1. muscle

>inspection

>inspection

>inspection

>inspection

>dark complexion with good skin turgor

>convex curvature

>prompt return of pink or usual color

>equal size on both sides of the body

LABORATORY AND DIAGNOSTIC EXAM URINALYSISDate Ordered: March 7, 2010Date Performed: March 10, 2010Microscopic ExamChemical ExamColor: Orange Albumin: TraceCharacteristic: Turbid Sugar: NegativeReaction pH: 5.0 (Normal: 7.35-7.45)Specific Gravity: 1.025 (Normal: 1.010-1.025)Bacteria: PositivePus Cells: 0.2Epithelial Cells: Moderate

HEMATOLOGYDate Performed: March 6, 2010ResultReference ValuesInterpretationSignificance

WBC14.53.5 10IncreasedIndicates presence of infection

HgB9.111.0 -16.5 g/dlDecreaseIndicates occurrence of anemia

Platelet170150 390 x 09/LDecreased

Differential Count

Lymphocytes42.217 - 48Normal

Monocytes11.32.0 6.0IncreasedIndicates presence of infection

Granulocytes56.543 - 76Normal

HEMATOLOGYDate Performed: March 8, 2010ResultReference ValuesInterpretationSignificance

WBC16.03.5 - 10IncreasedIndicates presence of infection

HgB8.811.0 -16.5 g/dlDecreaseIndicates occurrence of anemia

Platelet142150 390 x 09/LDecreasedIndicates hypercoagulation

Differential Count

Lymphocytes42.217 - 48Normal

Monocytes11.32.0 6.0IncreasedIndicates presence of infection

Granulocytes56.543 - 76Normal

Blood ChemistryDate Performed: March 8, 2010ResultReference ValuesInterpretationSignificance

Sodium132136 155Decreased

Potassium3.263.60 5.5Decreased

SerologyDate Performed: March 06, 2010TestResultMethod

HBsAGNon-ReactiveImmuno-chromatography

FecalysisPhysical Characteristic: SoftColor: YellowBacteria: WBC/HPF: 0 4RBC/HPF: Yeast CellsAmoeba: None found

REVIEW OF THE SYSTEMAnatomy and physiology of the liver

The liver is the largest internal organ in the body, and weighs about 3 pounds in an adult. The liver is located in the right upper quadrant of the abdomen, just below the diaphragm. A thick capsule of connective tissue called Glisson's capsule covers the entire surface of the liver. The liver is divided into a large right lobe and a smaller left lobe. The falciform ligament divides the two lobes of the liver. Each lobe is further divided into lobules that are approximately 2 mm high and 1 mm in circumference. These hepatic lobules are the functioning units of the liver. Each of the approximately 1 million lobules consists of a hexagonal row of hepatic cells called hepatocytes. The hepatocytes secrete bile into the bile channels and also perform a variety of metabolic functions. Between each row of hepatocytes are small cavities called sinusoids. Each sinusoid is lined with Kupffer cells, phagocytic cells that remove amino acids, nutrients, sugar, old red blood cells, bacteria and debris from the blood that flows through the sinusoids. The main functions of the sinusoids are to destroy old or defective red blood cells, to remove bacteria and foreign particles from the blood, and to detoxify toxins and other harmful substances. Approximately 1500 ml of blood enters the liver each minute, making it one of the most vascular organs in the body. Seventy-five percent of the blood flowing to the liver comes through the portal vein; the remaining 25% is oxygenated blood that is carried by the hepatic artery. The liver is responsible for important functions, including: Bile production and excretion Excretion of bilirubin, cholesterol, hormones, and drugs Metabolism of fats, proteins, and carbohydrates Enzyme activation Storage of glycogen, vitamins, and minerals Synthesis of plasma proteins, such as albumin and globulin, and clotting factors Blood detoxification and purification The liver synthesizes and transports bile pigments and bile salts that are needed for fat digestion. Bile is a combination of water, bile acids, bile pigments, cholesterol, bilirubin, phospholipids, potassium, sodium, and chloride. Primary bile acids are produced from cholesterol. When bile acids are converted or "conjugated" in the liver, they become bile salts. Bilirubin is the main bile pigment that is formed from the breakdown of heme in red blood cells. The broken-down heme travels to the liver, where is it secreted into the bile by the liver. Bilirubin production and excretion follow a specific pathway. When the reticuloendothelial system breaks down old red blood cells, bilirubin is one of the waste products. This "free bilirubin" is a lipid soluble form that must be made water-soluble to be excreted. The conjugation process in the liver converts the bilirubin from a fat-soluble to a water-soluble form. The liver also plays a major role in excreting cholesterol, hormones, and drugs from the body. The liver plays an important role in metabolizing nutrients such as carbohydrates, proteins, and fats. The liver helps metabolize carbohydrates in three ways: Through the process of glycogenesis, glucose, fructose, and galactose are converted to glycogen and stored in the liver. Through the process of glycogenolysis, the liver breaks down stored glycogen to maintain blood glucose levels when there is a decrease in carbohydrate intake. Through the process of gluconeogenesis, the liver synthesizes glucose from proteins or fats to maintain blood glucose levels. The liver synthesizes about 50 grams of protein each day, primarily in the form of albumin. Liver cells also chemically convert amino acids to produce ketoacids and ammonia, from which urea is formed and excreted in the urine. Digested fat is converted in the intestine to triglycerides, cholesterol, phospholipids, and lipoproteins. These substances are converted in the liver into glycerol and fatty acids, through a process known as ketogenesis. Prothrombin and fibrinogen, substances needed to help blood coagulate, are both produced by the liver. The liver also produces the anticoagulant heparin and releases vasopressor substances after hemorrhage. Liver cells protect the body from toxic injury by detoxifying potentially harmful substances. By making toxic substances more water soluble, they can be excreted from the body in the urine. The liver also has an important role in vitamin storage. High concentrations of riboflavin or Vitamin B1 are found in the liver. 95% of the body's vitamin A stores are concentrated in the liver. The liver also contains small amounts of Vitamin C, most of the body's Vitamin D stores, and Vitamins E and K.

COURSE IN THE WARDDate and TimePhysicians Order RationaleNursing Intervention

3/6/10* Please admit to FMW

* Secure consent

* BRAT DIET

* D5LRS 1l x 8hrs

* For fecalysis

* For CBC

* Therapeutics:Paracetamol 1 amp I.V. q 4hrs for temp. 38.5C

* Monitor V/S q 4 hrs

* I & O q Shift

* For confinement

* For legal purposes

* For rehydration and medication purposes

* For diagnostic purposes

* For further exams

* To lower body temperature during fever

* For baseline data

* For baseline data* Brought patient to FMW

* Secured consent for admission and management

* Administered as indicated by the physician

* Instructed patient to put a little amount of feces into a vial

* Explain to the patient why he needs to undergo for test

* Observed the 10 Rs in giving medication.

* Monitored V/S and recorded

* Monitored intake and output accordingly

Date and TimePhysicians Order RationaleNursing Intervention

3/7/10* TF: D5LRS 1L x 8 hrs

* Continue meds

* TF: D5LRS 1L x 8hrs

* Refer

* Clonidine 75 mg q 30mins x 3 doses if BP 140/90

* Amlodipine 5 mg 1 tab OD

* For rehydration and medication purposes

* For medication purposes

* For rehydration and medication purposes

* To provide immediate intervention for any complication the may arise

* Helps to lower blood pressure

* Helps to lower blood pressure* Administered as indicated by the physician

* Continue meds as indicated by the physician

* Continue meds as indicated by the physician

* Referred any problem to the physician

* Observed the 10 Rs in giving medication

* Observed the 10 Rs in giving medication

Date and TimePhysicians Order RationaleNursing Intervention

3/8/10* TF: D5NSS 1L x KVO

* Furosemide 40 mg I.V. q 12h

* Rpt CBC w/ APC

* For rehydration and medication purposes

* To facilitate urination as the patient has massive ascites* Continue infusion as prescribed by the physician

* Observed the 10 Rs in administering medication

Date and TimePhysicians Order RationaleNursing Intervention

3/9/10* TF: D5NSS 1L x 12h

* Refer UTZ of the whole abdomen* For rehydration and medication purposes

* * Continue infusion as prescribed by the physician

*

ALCOHOLIC LIVER DISEASE

ALCOHOLIC LIVER DISEASE

NURSING CARE PLANPatients name: Patient JAUNDICEAge: 48y.o.

AssessmentDiagnosisPlanningInterventionRationaleEvaluation

Subjective Data:Madi nga bumabbaba ti gurigor ko as verbalized by the patient.

Objective Data:-Weak appearance-Irritability-Warm to touch-Flushed skin-Temperature:38.9C

Hyperthermia related to pyrogenic effect secondary to bacterial infectionWithin 30minutes to 1hour of nursing intervention the patients temperature will decrease from 38.9C to 37C-Established rapport to the client through NPI

-Monitored temperature every 15minutes

-Provided TSB

-Advised patient to increase oral fluid intake

-Watched out for convulsions

-Advised S.O. to provide loose clothing to the patient

-Provided well room ventilation

-Administered paracetamol accurately as ordered by the physician and document-To build trust and cooperation of the patient and SO in the succeeding nursing interventions.

-To detect any alterations immediately.

-Facilitates heat loss by evaporation

-Increasing the fluid in the body boost its cooling system.

-Convulsion may cause complications

-Facilitates Heat loss by evaporation.

-To facilitate heat loss by convection

-Pharmacologic management for hyperthermia.After 1hour of nursing intervention the patients temperature decreased from 38.9C to 37C

-Goal met

NURSING CARE PLANAssessmentDiagnosisPlanningInterventionRationaleEvaluation

Subjective Data:

Nasakit toy tiyan ko as verbalized by the patient

Objective Data:

>Guarding behavior at the epigastric region>Irritability>Reduced interaction to people>Pain scale: 8/10

Acute pain related to abdominal cramping 2 to hyperperistalsisWithin 1 of nursing intervention the patient will manifest relaxation and no signs of pain.>Established rapport to the patient

>Encouraged S.O. to position the client in supine position with a warm heating pad on the abdomen

>Instructed S.O. to avoid giving hot and cold oral fluids

>Fixed bed linen free from wrinkles

>Provided calm environment

>Encouraged patient to have divertional activities like listening to music

>Encouraged relaxation technique such as deep breathing

>Watched out if pain scale increases

>Administered buscopan accurately as ordered by the physician and document

>To build trust

>These measures promote GI muscular relaxation and reduce cramping

>Cold liquid can induce cramping and hot liquid can stimulate peristalsis

>To provide comfort

>To promote nonpharmacological pain management

>Diverting attention will help to reduce pain

>This measure promote relaxation and helps divert pain

>Immediate increase in pain scale can be a cause of other complication> Pharmacologic management for abdominal pain.After 1 of nursing intervention the patient will manifest relaxation and no signs of pain.

-Goal met

DRUG STUDYDRUGCLASSIFICATIONROUTE/DOSAGEACTIONINDICATIONCONTRAINDICATIONADVERSE REACTIONNURSING CONSIDERATION

CIPROFLOXACIN

Antibacterial

500 mg/ 1 tab BID

Bactericidal; interferes with DNA replication in susceptible bacteria preventing cell reproduction.

For the treatment of infections caused by susceptible gram-negative bacteria, including Escherichia coli, Proteus mirabilis, Klebsiella pneumoniae, Enterobacter cloacae, Proteus vulgaris, Proteus rettgeri, Morganella morganii, Pseudomonas aeruginosa, Citrobacter freundii, Staphylococcus aureus, Staphylococcus epidermidis, group D streptococci Contraindicated with allergy to ciprofloxacin, norfloxacin or other fluoroquinolones, pregnancy, lactation. Use cautiously with renal impairment, seizures, tendinitis or tendon rupture associated with fluoroquinolone use.

CNS: Headache, dizziness, insomnia, fatigue, somnolence, depression, blurred vision, hallucinations, ataxia, nightmares CV: Arrhythmias, hypotension, angina EENT: Dry eye, eye pain, keratopathy GI: Nausea, vomiting, dry mouth, diarrhea, abdominal pain GU: Renal failure Hematologic: Elevated BUN, AST, ALT, serum creatinine and alkaline phosphatase; decreased WBC, neutrophil count, Hct History: Allergy to ciprofloxacin, norfloxacin or other quinolones; renal impairment; seizures; lactation Physical: Skin color, lesions; T; orientation, reflexes, affect; mucous membranes, bowel sounds; LFTs, renal function tests

DRUGCLASSIFICATIONROUTE/DOSAGEACTIONINDICATIONCONTRAINDICATIONADVERSE REACTIONNURSING CONSIDERATION

FUROSEMIDELoop Diurectic40 mg/ I.V. q12Inhibits reabsorption of sodium and chloride from the proximal and distal tubules and ascending limb of the loop of Henle, leading to a sodium-rich diuresis.Oral, IV: Edema associated with heart failure, cirrhosis, renal disease Contraindicated with allergy to furosemide, sulfonamides; allergy to tartrazine (in oral solution); anuria, severe renal failure; hepatic coma; pregnancy; lactation. Use cautiously with SLE, gout, diabetes mellitus.

CNS: Dizziness, vertigo, paresthesias, xanthopsia, weakness, headache, drowsiness, fatigue, blurred vision, tinnitus, irreversible hearing loss CV: Orthostatic hypotension, volume depletion, cardiac arrhythmias, thrombophlebitis Dermatologic: Photosensitivity, rash, pruritus, urticaria, purpura, exfoliative dermatitis, erythema multiforme

Profound diuresis with water and electrolyte depletion can occur; careful medical supervision is required. Administer with food or milk to prevent GI upset. Reduce dosage if given with other antihypertensives; readjust dosage gradually as BP responds. Give early in the day so that increased urination will not disturb sleep. Avoid IV use if oral use is at all possible.

DRUGCLASSIFICATIONROUTE/DOSAGEACTIONINDICATIONCONTRAINDICATIONADVERSE REACTIONNURSING CONSIDERATION

AMLODIPINEAntianginalAntihypertensiveCalcium channel blocker

5 mg /1 tab O.D.Inhibits the movement of calcium ions across the membranes of cardiac and arterial muscle cells; inhibits transmembrane calcium flow, which results in the depression of impulse formation in specialized cardiac pacemaker cells, slowing of the velocity of conduction of the cardiac impulse, depression of myocardial contractility, and dilation of coronary arteries and arterioles and peripheral arterioles; these effects lead to decreased cardiac work, decreased cardiac oxygen consumption, and in patients with vasospastic (Prinzmetals) angina, increased delivery of oxygen to cardiac cells. Angina pectoris due to coronary artery spasm (Prinzmetals variant angina) Chronic stable angina, alone or in combination with other drugs Essential hypertension, alone or in combination with other antihypertensives

Contraindicated with allergy to amlodipine, impaired hepatic or renal function, sick sinus syndrome, heart block (second or third degree), lactation. Use cautiously with heart failure, pregnancy.

CNS: Dizziness, lightheadedness, headache, asthenia, fatigue, lethargy CV: Peripheral edema, arrhythmias Dermatologic: Flushing, rash GI: Nausea, abdominal discomfort

Monitor patient carefully (BP, cardiac rhythm, and output) while adjusting drug to therapeutic dose; use special caution if patient has heart failure. Monitor BP very carefully if patient is also on nitrates. Monitor cardiac rhythm regularly during stabilization of dosage and periodically during long-term therapy. Administer drug without regard to meals.

DISCHARGE CARE PLAN

Medication Encouraged the patient to continue medications at home as prescribed by physician.

Emphasized the importance of taking medication as prescribed.

Exercise Encouraged patient to have daily exercise to reach optimum health recovery regarding condition.

Encouraged patient to have an adequate sleep and rest every day.

Treatment Emphasized the importance of adequate rest and sleep to prevent fatigue and avoid weight loss.

Advised the patient to continue taking medication as ordered on a regular basis.

Hygiene/Health Education Emphasized to the patient the importance of bathing and other hygienic procedure such as regular bathing to provide wellness and comfort.

Out-patient department Encouraged patient to visit the hospital if there were problems on heath or there is something that alters her health condition or visit the nearest health center or rural health unit for check-up to monitor her health condition.

Diet Instructed patient to have diet as tolerated. Instructed patient to eat nutritious food like vegetables, fruits and the like.

Spiritual Encouraged the patient to attend Sunday mass regularly and encouraged to pray for the safe and wellness of their health.

Research Paper helphttps://www.homeworkping.com/