Upper gastrointestinal dysfunction

– oral, oesophageal and gastric

Prepared by Gabrielle Metelli - 2009

University of Western Sydney

Objectives
¾ Identify common dysfunctions of the upper gastrointestinal tract
(GIT) – oral, oesophageal and gastric.
¾ Describe the risk factors that can lead to the development of these
dysfunctions.
¾ Identify causes, mechanism and treatment of upper GIT
dysfunctions.
¾ Describe the pathophysiology, clinical manifestations and treatment
for upper GIT dysfunctions.

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 MALNUTRITION
¾ Results from inadequate intake of nutrients.
¾ May be caused by
¾ Inadequate nutrient intake
¾ Impaired absorption and use of nutrients
¾ Loss of nutrients
¾ Increased metabolic needs

¾ Incidence & Prevalence

¾ Widespread cause of disease & mortality.

¾ It is estimated that approx. ½ of all hospitalised patients are

malnourished either on admission or develop due to surgery or
serious illness.
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¾ RISK FACTORS ¾ MANIFESTATIONS

¾ Age ¾ Weight loss
¾ Poverty, homelessness, inadequate ¾ Weakness, listlessness
food storage/preparation facilities ¾ Loss of subcutaneous fat
¾ Limited mobility/vision ¾ Muscle wasting/cramping
¾ Oral/GIT problems affecting food ¾ Thin/sparse hair
intake, digestion & absorption ¾ Flaking/dry/scaling/rough skin
¾ Inability to eat for ≥5 days ¾ Hepatomegaly
¾ Chronic pain/diseases ¾ Night blindness
¾ Dementia, mental health disorders ¾ Altered taste & smell
¾ Appetite affecting ¾ Confusion, apathy
medications/treatments
¾ Cardiomegaly, dyspnoea
¾ Alcohol/drug addiction
¾ Paresthesias, neuropathy, ataxia
¾ Acute problems – infection, surgery,
trauma ¾ Glossitis, stomatitis, swollen/bleeding
gums
¾ Delayed healing
¾ Easy bruising

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¾ Diagnosis ¾ Management

¾ Serum albumin & prealbumin ¾ Careful reintroduction of fluids

¾ Total lymphocyte count & nutrients to correct fluid &
¾ Serum electrolytes electrolyte imbalances
¾ Bioelectric impedance analysis ¾ Gradual introduction of protein
and calories
¾ Total daily energy expenditure
¾ Vitamin & mineral
supplements

¾ AIM – pt. to gain 1.5-

2kg/week
¾ Methods
¾ Enteral nutrition (tube)
¾ Parenteral nutrition (IV)
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Oral Cancer
¾ Oral cancer is a serious public health problem,
¾ with over 200,000 new cases reported annually worldwide,

¾ Two-thirds of which occur in developing countries.

¾ The overall mortality rate for intra-oral cancer remains high

¾ at approx. 50%, even with modern medical services,
¾
¾ Most likely due to the advanced stage of the disease at presentation.

¾ Major risk factors for oral cancer worldwide,

¾ notably tobacco, alcohol and betel quid

¾ Oral cancer predominantly affects

¾ the socially disadvantaged, residing in deprived areas.
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 Major Risk Factors for Oral Cancer
Tobacco Alcohol Betel Quid Dietary Factors
¾ >300 ¾ Alcohol has ¾Betel quid chewing produces ¾A low intake of fresh fruits &
carcinogens & local effects e.g., reactive oxygen species (ROS) vegetables is linked to an
pro-carcinogens direct actions on increased risk of oral cancer.
found in cell membranes, ¾These have multiple
tobacco smoke alteration in detrimental effects on oral ¾Vegetables & fruits that protect
or its water- mucosal mucosa. against oral cancer & pre-cancer
soluble permeability, are rich in b-carotene, vitamin C
compounds. variation in tissue & vitamin E with anti-oxidant
distribution and ¾ROS directly involved in
tumour initiation process, properties.
¾ These
contaminate ¾ systemic effects, ¾Iron deficiency can result in oral
saliva. e.g., nutritional ¾Induces genotoxicity & gene
mutation or attacks salivary epithelial atrophy & development
deficiencies, of cancer of upper airways and
immunological proteins & oral mucosa,
food passages
deficiencies &
disturbed liver ¾Leads to structural change in
function oral mucosa which allows ¾Dietary iron plays a protective
penetration by other BQ role in maintaining the thickness
ingredients & environmental of oral epithelium.
toxins.
¾Dietary fat & red meat may be
risk factors for cancer of head and
neck.
(Walker, Boey, & McDonald, 2003
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¾ Clinical Manifestations ¾ Treatment

¾ White patches ¾ Eliminate any causative factor/s

¾ Red patches ¾ Tumour staging then determines
¾ Ulcers therapy
¾ Masses ¾ Radiation therapy
¾ Pigmented areas ¾ Chemotherapy
¾ Fissures ¾ Surgery
¾ Asymmetry of head, face, jaws, or
neck

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 www.naturalypure.com
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Gastritis
¾ Definition
¾ inflammation of the gastric mucosa and one of the most common disorders of
the GIT system.

¾ acute or chronic.

¾ Can affect the fundus or antrium or both.

¾ Acute gastritis erodes the surface epithelium in a localised pattern

¾ often superficial.

¾ Can also be diffuse pattern of inflammation

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¾ ACUTE GASTRITIS
¾ Usually a result of injury of
protective mucosal barrier
¾ caused by drugs, IRR and
chemotherapy
¾ Short term inflammation
¾ Causes & contributing factors
¾ Alcohol,
¾ histamine,
¾ digitalis
¾ metabolic disorders - uraemia
(associated with renal/respiratory
failure or cirrhosis).
¾ Highest incidence - men in the 5th
and 6th decades of life.
¾ CHRONIC GASTRITIS
¾ 3 FORMS : gastric secretion
progressively fails
¾ SUPERFICIAL – marked
inflammation causes
¾ reddened, oedematous mucosa with
small erosions and haemorrhage.
¾ ATROPHIC – occurs in all layers &
frequently develops in association
with gastric ulcer & gastric cancer.
¾ Characterized by a decreased no. of
parietal & chief cells.
¾ HYPERTROPHIC – produces dull &
nodular mucosa with irregular,
thickened or nodular rugae –
hemorrhages occur frequently.

¾ Incidence greater in smokers and

heavy drinkers,
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ETIOLOGY & RISK FACTORS - chronic

¾ PUD
¾ infection with Helibactor pylori
¾ this can lead to gastric cancer.

¾ Gastric surgery
¾ bile and acids may reflux into the remaining stomach, causing
gastritis.

¾ Age

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 Pathophysiology
¾ Acute Gastritis
¾ Mucosal lining of the stomach is
protected against the HCl.
¾If barrier penetrated, mucosa
becomes injured.
¾ HCl comes in contact with the
mucosa, injury to small
vessels occurs
¾oedema, hemorrhage and
possible ulcer formation.
¾ Damage assoc. with acute gastritis
is usually limited.
¾ Damage to the mucosa can occur
within minutes
¾ outcome depends upon the
severity and extent of the
damage.
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¾ Chronic Gastritis
¾ In the beginning – similar to acute
gastritis.
¾ Lining first becomes thick and red
and then thin and atrophic.
¾ Atrophy causes loss of function
¾ When acid decreases the source of
intrinsic factor is lost.
¾ Ulcers and bleeding can occur
resulting in minimal
amounts of acid secreted
(achlohydria) a predisposer
to gastric cancer.
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CLINICAL MANIFESTATIONS
¾ Acute Gastritis ¾ Chronic Gastritis
¾ Abdominal tenderness ¾ S & S may be vague and even
¾ epigastric discomfort absent
¾ cramping
¾ Belching ¾ no increase in the secretion of HCl,
¾ reflux & severe n/v
¾ Headache & Low grade fever ¾ anorexia, feeling of fullness,
¾ If contaminated food diarrhoea within
5 hours of ingestion ¾ belching, nausea,
¾ malaise
¾ epigastric pain or intolerance to
¾ Potent corrosive chemical can cause
peritonitis spicy foods.
¾ Painless GI bleeding
¾ Malaena.
¾ sometimes haematemesis
¾ haemorrhage (tachycardia,
hypotension, vertigo, restlessness,
pallor)

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¾ Diagnostic tests - acute ¾ Diagnostic tests - chronic
¾ Stool (occult) test
¾ FBC,
¾ Full blood test-Hb and
hematocrit ¾ Vit B12,
(inflammation, ¾ endoscopy.
haemorrhage) ¾ Stool (occult) test
¾ Endoscopy- oesophago-gastro-
¾ Detailed history of food and
duodenoscopy medications
¾ Endoscopy- oesophago-gastro-
¾ Gastric analysis to assess duodenoscopy
hydrochloric acid
secretion

¾B12 levels

¾ Detailed history of food and

medications

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MANAGEMENT
¾ Chronic
¾ Acute
¾ Diagnosis – rule out gastric cancer.
¾ Remove the cause.
¾ Diet – client eats what suits them,
¾ Treat the vomiting small frequent meals
¾ Antacids or histamine(H2) ¾ Lifestyle education – stop smoking,
receptor antagonists NBM until reduce alcohol, decrease caffeine,
vomiting subsides regular check ups
¾ Liquid diet and liquid antacids ¾ Antacids – Mylanta to relieve
¾ IV therapy discomfort
¾ Return to normal diet when ¾ H.pylori – a combination of drugs –
feeling able Losec, Flagyl. Regime given over a
¾ Gastric lavage week and can be repeated.
¾ Prevent complications- ¾ Vit B12 (for life, Cobalamin),
haemorrhage and peritonitis corticosteroids (attempt to regenerate
parietal cells), ranitidine are often
ordered.
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 COMPLICATIONS - chronic
¾ Bleeding
¾ Pernicious Anaemia
¾ lack of intrinsic factor.
¾ B12 needed in formation of RBC, nerve cell function – (fatigue, parathesias,
SOB, diarrhoea, ataxia
¾ Gastric cancer - adenocarcinoma

SURGICAL MANAGEMENT
Surgery may be required to control the bleeding
¾ subtotal gastrectomy
¾ (partial removal of the stomach)
¾ Pyloroplasty
¾ widening of the pylorus enhancing gastric emptying.
¾ Vagotomy
¾ cutting of the right and left vagus nerves – eliminates acid-secreting stimulus to
the gastric cells.
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PEPTIC ULCER DISEASE

¾ Involves a break in the continuity of the oesophageal, gastric or
duodenal mucosa.

¾ Corrosive action of HCl and pepsins in the gastric secretions on the

exposed mucosa cause necrosis and ulceration

¾ Occurs in any part of the GI tract in contact with gastric juices.

¾ Occurs in approx. 10% of the population.

¾ Men more likely to have gastric and duodenal ulcers.

¾ Acute / chronic – gastric / duodenal

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 DUODENAL ULCERS
¾ Greater incidence
¾ Hypersecretion of acid is the
greatest cause.
¾ Clients with a duodenal ulcer
experience low pH levels in the
duodenum for longer periods –
¾ the stomach lining is more sensitive
to gastrin & secretes excess gastrin
¾ More rapid gastric emptying occurs
and
¾ in combination with hypersecretion
causes large acid load in duodenum.
GASTRIC ULCERS
¾ Most common area - within 2.5cm
of the pylous
¾ these heal within weeks.
¾ Cause
¾ break in the mucosa.
¾ Incompetent pylorus may decrease
the production of mucus
¾ which allows reflux of bile into the
stomach (corrosive).
¾ Decreased blood flow to the gastric
mucosa may also alter the
defensive barrier
¾ leading to breaks in the mucosa.

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ETIOLOGY AND RISK FACTORS

¾ H.pylori – cause in almost 90% of all peptic ulcers.
¾ Ulceration occurs when aggressive factors exceed the defensive barrier.
¾ Risk factors – NSAID, steroids, smoking, caffeine, stress and alcohol

PATHOPHYSIOLOGY
¾ 2 different mechanisms for development of PUD :
¾ breakdown of the protective epithelial lining
¾ Stress

¾ Zollinger –Ellison syndrome is characterised by abnormal secretion of

gastrin by a rare islet tumor in the pancreas.
¾ These clients have diarrhoea secondary to fat malabsorption - steatorrhea.
¾ Treatment is aimed at suppression of acid secretion.

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health.yahoo.com/topic/digestive/overview/ar

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Clinical Manifestations
¾ GASTRIC ¾ DUODENAL

¾ Pain on eating, can be variable ¾ Pain on empty stomach

¾ Antacids ineffective ¾ Relieved by food and antacids
¾ Usually well nourished ¾ Often malnourished
¾ Haematemesis more common ¾ Malaena more common than
than malaena haematemesis
¾ Recurrence unlikely after surgery ¾ Recurrence as marginal ulcers
after surgery

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 DIAGNOSIS
¾ Clinical manifestations
¾ Endoscopy and biopsy
¾ FBC
¾ testing for H.pylori – via urea breath tests

MANAGEMENT
¾ Provide rest for the stomach
¾ H.pylori – use medication regime
¾ Reduce gastric secretions
¾ Strengthen mucosal barrier
¾ Diet

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COMPLICATIONS SURGERY
¾ Haemorrhage ¾ Subtotal gastrectomy
¾ Pyloroplasty
¾ Treatment for shock
¾ Vagotomy 3 types:
¾ Vasopression – for haemorrhage
¾ Truncal
¾ Rest – administer analgesia
¾ Selective
¾ PERFORATION – a surgical
emergency ¾ Proximal
¾ Surgery ¾ Gastrectomy
¾ Pain ¾ Gastroenterostomy
¾ IV fluids
¾ IV antibiotics +++++ ¾ Antrectomy

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 Bibliography
¾ Black, J. M., Hawks, J., & Keene, A. M. (2004). Medical-surgical nursing: Clinical
management. (7th ed.). Philadelphia: W. B. Saunders.

¾ Lehne, R. A .(2007). Pharmacology for nursing care. (6th ed.). St.Louis: Saunders
Elsevier.

¾ Lemone, P., & Burke, K. (2007). Medical surgical nursing. Critical thinking
in client care. (4th ed.). Upper Saddle River, New Jersey:Prentice Hall.

¾ Lemone, P., & Burke, K. (2004). Medical surgical nursing. Critical thinking
in client care. (3rd ed.). Upper Saddle River, New Jersey:Prentice Hall.

¾ McCance, K. L., & Heuther, S. E. (2002). Pathophysiology: The biologic basis for
disease in adults and children. (4th ed.). St. Louis : C.V.Mosby.

¾ Walker, D., Boey, G., & McDonald, L. (2003). The pathology of oral cancer.
Pathology, 35(5), 376-383.

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