Thedi

Group 18 Problem 1B

Thedi Darma Wijaya405090120

LO 1: Anatomy, Histology, Physiology, and Biochemical of

Upper GIT

Anatomy of Upper GIT

Cavum Oris; Oral Or Buccal Cavity

•  The Palate (palatum) forms the roof of the mouth; it consists of two portions– the hard palate in

front– the soft palate

behind.

• The Teeth (dentes)– The deciduous teeth are twenty

in number: • four incisors, two canines, and four

molars, in each jaw.  – The permanent teeth are thirty-

two in number: • four incisors, two canines, four

premolars, and six molars, in each jaw.

• The Salivary Glands– Three large pairs

of salivary glands communicate with the mouth, and pour their secretion into its cavity; they are

• The parotid, • The

submaxillary, • The

sublingual.

The Esophagus• The esophagus or gullet is

a muscular canal, about 23 to 25 cm. long, extending from the pharynx to the stomach.

• There are 3 portions of esophagus:– The cervical portion– The thoracic portion– The abdominal portion

• It measures about 1.25 cm. in length.

• It is somewhat conical with its base applied to the upper orifice of the stomach, and is known as the antrum cardiacum.

The Abdomen

• a. Median plane.• b. Lateral planes.• c. Trans tubercular

plane.• d. Subcostal plane.• e. Transpyloric plane

The abdominal Regions

The Peritoneum

The Stomach

• Muscular layers of stomach

The Duodenum• The Duodenum has received its name from

being about equal in length to the breadth of twelve fingers (25 cm.)

• The duodenum may be divided into four portions: superior, descending, horizontal, and ascending.

Histology of Upper GIT

The layers of GIT• a. Fibrous covering.• b. Divided fibers of longitudinal

muscular coat. • c. Circular muscular fibers. • d. Submucous or areolar layer. • e. Muscularis mucosæ. • f. Mucous membrane, with

vessels and part of a lymphoid nodule.

• g. Stratified epithelial lining. • h. Mucous gland. • i. Gland duct.

The oesophagus• The oesophagus has a stratified

squamous epithelial lining (SE) which protects the oesophagus from trauma

• The submucosa (SM) secretes mucus from mucous glands (MG) which aid the passage of food down the oesophagus.

• The lumen of the oesophagus is surrounded by layers of muscle (M)- voluntary in the top third, progressing to involuntary in the bottom third- and food is propelled into the stomach by waves of peristalisis.

The Stomach• G- mucosa containing glandular

tissue:– parietal cells which secrete

hydrochloric acid– chief cells which secrete pepsin– enteroendocrine cells which secrete

regulatory hormones.• MM- muscularis mucosae • SM- submucosa • The stomach contains three layers

of involuntary smooth muscle :– OM- inner oblique muscle – CM- circular muscle – LM- outer longditudional muscle

The Small Intestine• The epithelial surface of the

plicae (P) is further folded to form villi(V), the surface of each villus is covered in small microvilli to maximise surface area- the area available for absorption is vast.

• The vessels can be seen in the submucosa (SM)

• The double muscle layer (M) moves food through the intestine by peristalisis.

The large Intestine• The mucosa (M) is arranged into

tightly-packed straight tubular glands (G) which consist of cells specialised for water absorption and mucus-secreting goblet cells to aid the passage of faeces.

• The large intestine also contains areas of lymphoid tissue (L); these can be found in the ileum too (called Peyer's patches), and they provide local immunological protection.

Physiology & Biochemical of Upper GIT

LO 2: Nausea & Vomiting Patophysiology

Physiology of nausea and vomiting• The vomiting reflex is triggered by stimulation of chemoreceptors in the

upper GI tract and mechanoreceptors in the wall of the GI tract which are activated by both contraction and distension of the gut as well as by physical damage.

• A coordinating center in the central nervous system controls the emetic response. This center is located in the parvicellular reticular formation in the lateral medullary region of the brain.

• Afferent nerves to the vomiting center arise from abdominal splanchnic and vagal nerves, vestibulo-labyrinthine receptors, the cerebral cortex and the chemoreceptor trigger zone (CTZ).The CTZ lies adjacent in the area postrema and contains chemoreceptors that sample both blood and cerebrospinal fluid.

• Direct links exist between the emetic center and the CTZ. The CTZ is exposed to emetic stimuli of endogenous origin such as hormones associated with pregnancy and to stimuli of exogenous origin such as drugs (3).

• The efferent branches of cranial nerves V, VII, and IX, as well as the vagus nerve and sympathetic trunk produce the complex coordinated set of muscular contractions, cardiovascular responses and reverse peristalsis that characterizes vomiting

LO 3: Diseases in Upper GIT

GERD

• GERD is one of the most prevalent gastrointestinal disorders.

• Population-based studies show that up to 15% of individuals have heartburn and/or regurgitation at least once a week, and 7% have symptoms daily.

• Symptoms are caused by backflow of gastric acid and other gastric contents into the esophagus due to incompetent barriers at the gastroesophageal junction.

Risk Factor• Incompetence of the diaphragmatic crural

muscle, which surrounds the esophageal hiatus in the diaphragm and functions as an external LES, also predisposes to GERD.

• Obesity is a risk factor for GERD.

Pathophysiology• Reflux occurs only when the gradient of pressure between the

LES and the stomach is lost. • It can be caused by a sustained or transient decrease in LES

tone. • Secondary causes of sustained LES incompetence include

scleroderma-like diseases, myopathy associated with chronic intestinal pseudo-obstruction, pregnancy, smoking, anticholinergic drugs, smooth-muscle relaxants ( -adrenergic agents, aminophylline, nitrates, calcium channel blockers, and phosphodiesterase inhibitors), surgical damage to the LES, and esophagitis.

Pathophysiology• tLESR without associated esophageal contraction is

due to a vagovagal reflex in which LES relaxation is elicited by gastric distention.

• Increased episodes of tLESR are associated with GERD.

• Apart from incompetent barriers, gastric contents are most likely to reflux – (1) when gastric volume is increased (after meals, in pyloric

obstruction, in gastric stasis, during acid hypersecretion states),

– (2) when gastric contents are near the gastroesophageal junction (in recumbency, bending down, hiatal hernia), and

– (3) when gastric pressure is increased (obesity, pregnancy, ascites, tight clothes).

Clinical Features• Heartburn and regurgitation of sour material into the mouth are

the characteristic symptoms of GERD. • Angina-like or atypical chest pain occurs in some patients. • Persistent dysphagia suggests development of a peptic

stricture. – Most patients with peptic stricture have a history of several years of

heartburn preceding dysphagia. • Rapidly progressive dysphagia and weight loss may indicate

the development of adenocarcinoma in Barrett's esophagus. • Bleeding occurs due to mucosal erosions or Barrett's ulcer. • Extraesophageal manifestations : chronic cough, laryngitis, and

pharyngitis. • Recurrent pulmonary aspiration may cause or aggravate

chronic bronchitis, asthma, pulmonary fibrosis, chronic obstructive pulmonary disease, or pneumonia.

• Chronic sinusitis and dental decay have also been ascribed to GERD.

Diagnosis• The diagnosis can be made by history alone in many cases. • A therapeutic trial with a PPI such as omeprazole, 40 mg bid for

1 week, provides support for the diagnosis of GERD.• The diagnostic approach to GERD can be divided into three

categories: – (1) documentation of mucosal injury,

• by the use of barium swallow, esophagoscopy, and mucosal biopsy

– (2) documentation and quantitation of reflux• can be done by ambulatory long-term (24–48 h)

esophageal pH recording – (3) definition of the pathophysiology.

• indicated for management decisions such as antireflux surgery

Treatment • The goals of treatment are to provide symptom relief,

heal erosive esophagitis, and prevent complications • Pharmacology

– H2 receptor blocking agents (cimetidine, 300 mg qid; ranitidine, 150 mg bid; famotidine, 20 mg bid; nizatidine, 150 mg bid) are effective in symptom relief.

– PPIs are more effective and more commonly used.• The PPIs are comparably effective: omeprazole (20 mg/d),

lansoprazole (30 mg/d), pantoprazole (40 mg/d), esomeprazole (40 mg/d), or rabeprazole (20 mg/d) for 8 weeks can heal erosive esophagitis in up to 90% of patients. The PPI should be taken 30 min before breakfast.

• SE: hypergastrinemia but does not increase the risk for carcinoid tumors or gastrinomas. Vitamin B12 and calcium absorption may be compromised

Treatment • Non Pharmacology

– The management of mild cases includes weight reduction, sleeping with the head of the bed elevated by about 4–6 in. with blocks, and elimination of factors that increase abdominal pressure.

– Patients should not smoke and should avoid consuming fatty foods, coffee, chocolate, alcohol, mint, orange juice, and certain medications (such as anticholinergic drugs, calcium channel blockers, and other smooth-muscle relaxants).

– They should also avoid ingesting large quantities of fluids with meals.

– Patients who have an associated peptic stricture are treated with endoscopic dilation to relieve dysphagia, and such patients should be vigorously treated for reflux.

– Esophagoscopy should also be performed in patients suspected of other complications such as bleeding or development of cancer.

Peptic Ulcer Disease

Definition • Burning epigastric pain exacerbated by fasting

and improved with meals is a symptom complex associated with peptic ulcer disease (PUD).

• An ulcer is defined as disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation.

• Ulcers are defined as breaks in the mucosal surface >5 mm in size, with depth to the submucosa.

• Ulcers occur within the stomach and/or duodenum and are often chronic in nature

Epidemiology• Duodenal Ulcers• DUs are estimated to occur in 6–15% of the Western

population. • The death rates, need for surgery, and physician visits have

decreased by >50% over the past 30 years. • The reason for the reduction in the frequency of DUs is likely

related to the decreasing frequency of Helicobacter pylori.• Eradication of H. pylori has greatly reduced these recurrence

rates.• Gastric Ulcers• GUs tend to occur later in life than duodenal lesions, with a

peak incidence reported in the sixth decade. • More than half of GUs occur in males and are less common

than DUs, perhaps due to the higher likelihood of GUs being silent and presenting only after a complication develops..

Pathology• Duodenal Ulcers• DUs occur most often in the first portion of duodenum (>95%),

with ~90% located within 3 cm of the pylorus. • They are usually 1 cm in diameter but can occasionally reach

3–6 cm (giant ulcer). • Ulcers are sharply demarcated, with depth at times reaching

the muscularis propria. • The base of the ulcer often consists of a zone of eosinophilic

necrosis with surrounding fibrosis.• Gastric Ulcers• In contrast to DUs, GUs can represent a malignancy.• Benign GUs are most often found distal to the junction between

the antrum and the acid secretory mucosa. • Benign GUs associated with H. pylori are also associated with

antral gastritis.

Pathophysiology• Duodenal Ulcers• H. pylori and NSAID-induced injury account for the majority of

DUs. • Many acid secretory abnormalities have been described in DU

patients. • Bicarbonate secretion is significantly decreased in the

duodenal bulb of patients with an active DU as compared to control subjects.

• H. pylori infection may also play a role in this process

Pathophysiology• Gastric Ulcers• GUs that occur in the prepyloric area or those in the

body associated with a DU or a duodenal scar are similar in pathogenesis to DUs.

• Gastric acid output (basal and stimulated) tends to be normal or decreased in GU patients.

• When GUs develop in the presence of minimal acid levels, impairment of mucosal defense factors may be present.

• Abnormalities in resting and stimulated pyloric sphincter pressure with a concomitant increase in duodenal gastric reflux have been implicated in some GU patients.

Pathophysiology• H. pylori and Acid Peptic Disorders• Gastric infection with the bacterium H. pylori

accounts for the majority of PUD. This organism also plays a role in the development of gastric mucosal-associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma

Clinical Features • Epigastric pain described as a burning or gnawing

discomfort can be present in both DU and GU• Pain that awakes the patient from sleep (between

midnight and 3 A.M.) is the most discriminating symptom, with two-thirds of DU patients describing this complaint.

• The pain pattern in GU patients may be different from that in DU patients, where discomfort may actually be precipitated by food.

• Nausea and weight loss occur more commonly in GU patients.

• Dyspepsia.

Physical Examination• Epigastric tenderness is the most frequent

finding in patients with GU or DU. • Physical examination is critically important for

discovering evidence of ulcer complication.• Tachycardia and orthostasis suggest

dehydration secondary to vomiting or active gastrointestinal blood loss.

• A severely tender, boardlike abdomen suggests a perforation.

• Presence of a succussion splash indicates retained fluid in the stomach, suggesting gastric outlet obstruction.

Drugs Used in the Treatment of Peptic Ulcer DiseaseDrug Type/Mechanism Examples DoseAcid-suppressing drugs    

  Antacids Mylanta, Maalox, Tums, Gaviscon

100–140 meq/L 1 and 3 h after meals and hs

  H2 receptor antagonists 

Cimetidine Ranitidine Famotidine Nizatidine

400 mg bid300 mg hs40 mg hs300 mg hs

  Proton pump inhibitors Omeprazole Lansoprazole Rabeprazole Pantoprazole Esomeprazole

20 mg/d30 mg/d20 mg/d40 mg/d20 mg/d

Mucosal protective agents

  Sucralfate Sucralfate 1 g qid

  Prostaglandin analogue

Misoprostol 200     g qid

  Bismuth-containing compounds

Bismuth subsalicylate (BSS)

See anti-H. pylori regimens (Table 287-4)

• www. Theodora.com/anatomy• Harrison• Anatomi Abdomen• Medscape.com