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Gastroesophageal reflux disease (GERD), Gastric reflux disease, or Acid reflux disease is defined as chronic symptoms or mucosal damage produced by the abnormal reflux in the esophagus. This is commonly due to transient or permanent changes in the barrier between the esophagus and the stomach. This can be due to incompetence of the lower esophageal sphincter, transient lower esophageal sphincter relaxation, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia
This is a case of DC a 68 yr. old female residing at Kabihasnan., the patient was received at PCH last July 22, 2009 at 05:39 pm with a chief complaint of D.O.B and Abdominal pain. Initial vital signs were taken BP -90/60, T-36.3˚C, RR- 30 cpm, PR110 bpm. Initial diagnosis was(G.E.R.D) Gastroesopageal reflux disease. The patient was subjected for ECG, Na, K+, CBC, and urinalysis and was given Ranitidine,
Domperidone, esomeprazole, hydryt and Kalium as prescribed.
To be able to know the comprehensive process of the disease condition Specific Objectives To be able to perform or identify the patient in response to the disease condition
To be able to discuss the normal anatomy and physiology To be able to trace the pathophysiology of the Disease To be able to know comprehensively the laboratory examinations, diagnostic
examinations and the treatment accompanied to the disease process of G.E.R.D To be able to assimilate all the learning experience garnered with this case study
To be able to formulate an efficient and effective Nursing Care Plan
Name: DC Age: 68 Gender: Female Civil Status: Married Date of Birth: December 8 1940 Address: kabihasnan Place of Birth: Parañaque Reiligion: Roman Catholic Educational Attainment: Highschool Language Spoken: Tagalog Admitting Diagnosis/Impression: Community Acquired Pneumonia (Moderate to high risk) Admitting Physician: Dr. Karishma Sumilin
NURSING HISTORY Chief Complaint: Difficulty of breathing
History of present illness: 1 days prior to admission patient experience acute
pain, radiating upward(heartburn) with associated pericardial pain.
PAST MEDICAL HISTORY Immunization status: not complete Hospitalization: Fever FAMILY HEALTH HISTORY Health Stage and ages of (cause of death) Siblings: none Spouse: none
Date Performed: July 22, 2009 1. Measurement: 1.1 Weight: 54 kgs 1.2 Vital Signs: No. Of Hospital Days: 1 days Height: 5’4
Temperature: 36.3 0C
2. General Appearance
PR: 110 bpm
RR: 30 cpm
BP: 90/60 mmHg
The Client is conscious, coherent and oriented to place and person. Looks according to his age. 3. Skin Inspection: General color of the skin is brown, uniform in color except on part not exposed to the sun. Palpation: Skin is dry with poor skin turgor; with flush skin and warm to touch. 4. Head Inspection: Normocepahalic, appears round, evenly distributed hair with no dandruff, lesions and infestations. Palpation: No mass noted. 5. Eyes Inspection: Eyes are symmetrical, the conjunctiva is pink and with anicteric sclera. Cornea and lens are smooth and clear. Pupil is equally round and reactive to light. 6. Ears Inspection: Symmetrical and proportional to the head. The external canal has no purulent discharge.
Palpation: Upon palpation, both ears are non-tender with no presence of mass or nodules. 7. Nose Inspection: Nasal folds are symmetrical. Nasal septum is located at the midline. Mucosa is pink and moist, and intact without presence of discharge. Palpation: Airways are patent on both nasal nares. No tenderness on frontal and maxillary sinuses. 8. Mouth Inspection: Upon inspection of the mouth, the lips are pinkish and dry with tongue located at the midline. Gums and mucosa are pinkish and with missing teeth. 9. Pharynx
Inspection: Uvula is midline. Right tonsils and posterior pharyngeal wall are not inflamed. 10. Neck Inspection: Neck is symmetrical with full range of motion. No visible deformities seen Palpation: Trachea is midline. No swelling and tenderness of lymph nodes noted. Thyroid gland is non-palpable, no mass noted.
11. Chest and Lungs Inspection: Shape of the chest is symmetrical. No lesions noted. I&E ratio is 1:2 with dyspnea. Palpation: Anterior-Posterior-Lateral ratio is 1:2 with symmetrical lung expansion and symmetrical vocal/tactile fremitus. Percussion: The sound of resonance was found at the 1st to 4th ICS and dullness at left 5th ICS midclavicular line. Auscultation: Bronchial sound is heard over trachea, bronchovesicular sound at 2nd and 3rd ICS and vesicular sound at the base of the lung. With crackles heard on the lower posterior back.
12. Heart Inspection: Precordium is normo-dynamic Palpation: No presence of abnormal pulsations at precordium
Auscultation: The point of maximum impulse is located at the 5th ICS MCL with regular heart rhythm. Heart sounds S1 is louder at the apex; S2 is louder at the base. No extra heart sound noted. 13. Breasts and Axillae Area: (NOT ASSESSED) 14. Abdomen Inspection: The client’s abdomen is flat with symmetrical configuration. No scars, lesions, striae noted. The color of the skin is slightly lighter than those areas exposed to sun. Auscultation: Bowel sound was normoactive. Percussion: Tympanic sounds are heard over areas of RLQ and LLQ. Dullness was heard over RUQ (liver), dullness over LUQ (spleen) Palpation: There was no tenderness when palpated. 15. Genito-Urinary System: (NOT ASSESSED)
ANATOMY The esophagus is a member of the digestive tract whose main responsibility is to transfer food
from the pharynx to the stomach. It measures about 10 inches in length and is tubular and collapsible. The esophagus can be traced from the originating point of the larynx running behind the trachea. It traces down the mediastinum of the thorax until it runs into the diaphragm, ending just above the stomach’s opening. The esophageal hiatus refers to the opening in the diaphragm. Nonkeratinized stratified squamous epithelium lines the esophagus. The walls themselves are either created by skeletal muscles or by smooth muscle tissue. Skeletal muscle lines the upper 1/3 of the esophagus, while the middle 1/3 is a combination of the two muscle tissues, leaving the remaining 1/3 as smooth muscle tissue. Where the stomach and the esophagus meet, there is a thickening of the circular muscle fibers, creating the gastroesophageal sphincter, or the lower esophageal sphincter. This sphincter is responsible for maintaining the food and fluids inside the stomach, preventing regurgitation up into the esophagus. Air in the lungs creates an additional pressure in the lower thoracic region, encouraging regurgitation of foods and fluids.
The Mechanisms of Swallowing Deglutition is the term given to the process of swallowing, a highly mechanical and functionally complex process that allows the initiation of digestion to occur. Deglutition is typically described in three basic phases, allowing for clarity. The initial stage of deglutition is preceded by mastication if there is a solid in the process. This is a voluntary stage, meaning that a human must begin this stage consciously. The oral cavity closes and the process of breathing is temporarily suspended. The bolus has been formed through
the process of mastication, and the tongue then lifts the bolus firm against the transverse palatine folds of the hard palate. The mylohyoid muscle and the styloglossus muscle contract to produce this experience. The secondary stage takes over from this point, passing the bolus through the pharynx. The second stage of deglutition is involuntary. Sensory receptors that are positioned at the opening of the oropharynx stimulate the secondary action. The tongue is pressing the bolus against the transverse palatine folds of the hard palate, which creates a seal against the nasopharynx. This not only prevents the bolus from entering the airway, but it also stimulates the pressure senses of the oropharynx and forces the bolus into the opening. The soft palate along with the uvula close off the rest of the nasopharynx while the bolus passes into the gullet, and the hyoid bone and the larynx elevate protectively. The constrictor muscles of the pharynx then contract in a rhythmic and intentional sequence in order to force the bolus through the pharynx, where it will then enter the esophagus. This entire stage can be completed in less then a second. The final stage of deglutition is also involuntary, and it deals specifically with the bolus entering and passing through the esophagus. Peristalsis kicks in naturally and the bolus in pressured down the esophagus. Fluids are rushed through this entire process, all three stages, in under a second,
while an average sized bolus takes approximately 5 to 8 seconds to complete the three stages.
Pathophysiology The development of GE reflux disease depends on a combination of the following four factors: (1) defective anti-reflux mechanism, (2) the presence of caustic gastric contents, (3) poor esophageal clearance, (4) diminished esophageal mucosal resistance. 1) Anti-reflux mechanism As intra-abdominal pressure is always greater than intrathoracic pressure, if it were not for an anti-reflux barrier, GE reflux would be occurring almost constantly. The role of the esophageal sphincter refers to a segment of specialized circular mucosa at the GE junction approximately 3 cm in length which maintains a pressure 10 mmHg to 40 mmHg higher than the pressure of the stomach thereby preventing GE reflux. Before the advent of widespread use of esophageal manometry, primary LES hypotonia was felt to account for all cases of GE reflux disease. Using modern manometric techniques, however, it has been demonstrated that only the minority (10-20%) of patients with GE reflux disease do in fact have lower than normal LES pressures. It is now believed by most investigators that the presence of transient LES relaxation explains GE reflux in the majority of patients. Normally the LES relaxes briefly after a peristaltic wave to allow passage of the bolus from the esophagus into the stomach. Transient LES relaxation refers to inappropriate relaxation of the sphincter occurring without a preceding peristaltic wave and lasting up to 30 seconds in duration. These transient sphincter relaxations allow for reflux of caustic gastric contents into the esophageal body. The presence of a hiatus hernia, originally felt to be central in the pathogenesis of GERD has continued to be the subject of much debate and controversy. Many patients have GERD in the absence of hiatus hernias, and only the minority of patients with hiatus hernias develop GE reflux. Recent studies on cats and human beings have shown that the crural diaphragm does play a role in maintaining basal LES pressure. It is unclear, however, how important a factor this is in most patients for maintaining LES competence. 2) Gastric Contents In order for gastroesophageal reflux to result in esophageal damage and symptomatic heartburn there must be material in the stomach which is caustic to esophageal mucosa. Clearly acid present in the stomach is the primary caustic agent, underscored
by the dramatic improvement almost all patients feel and endoscopic exam demonstrates in patients with severe esophagitis. The role of other caustic agents such as pepsin, bile salts, pancreatic enzymes and bicarbonate is less clear. People with GE reflux disease have not been shown to be hypersecreters of gastric acid, however, patients with delayed gastric emptying either on the basis of pyloric stenosis or gastroparesis frequently develop resultant severe GE reflux. 3) Esophageal Clearance In order for the caustic reflux to cause tissue damage it must be in contact with the mucosa for a sufficient period of time. Normally refluxed material is cleared by a combination of gravity and secondary peristalsis. In patients with disordered esophageal peristalsis, particularly scleroderma, the material refluxed into the esophagus has the opportunity to have prolonged contact with the esophageal mucosa thereby causing severe erosive damage especially when the patient is supine. Additionally important clearance is salivary and esophageal bicarbonate formation which helps neutralize the refluxed acid. 4) Esophageal Mucosal Resistance A more recently identified and poorly understood component of the defensive mechanism in preventing GERD is esophageal mucosal resistance. The factors involved in esophageal mucosal resistance to acid are much less well understood and much more poorly developed than mucosal resistance factors of the stomach. What is known, however, is that patients can develop erosive esophagitis in the setting of very minimal GE reflux documented by a 24 hour pH probe, and on the other hand there are patients with severe GE reflux as documented on pH probe which do not develop significant esophageal damage. Cheap canadian pharmacy
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