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Dr.
KARRENBERG’S 2011 NCLEX-RN®
ONLINE - Tutorial and Review Class
NCLEX-RN ® Category III,IV,V:
GASTROINTESTINAL TRACT DISORDERS AND DISEASES
Subject
materials:
Clicking on the individual topics and keywords will refer
you to the rationales on this page.
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back to this menu.
Gastrointestinal
Tract Disorders and Diseases
Gastroesophageal Reflux Disease (GERD)
Chronic
inflammatory bowel diseases
Irritable
bowel syndrome (IBS)
Disorders
and Diseases of the Liver
Pathophysiology
of liver failure
Gallbladder
and biliary duct disorders
Gastrointestinal
Tract Medication Therapy
Audio files and
Diagrams are implemented throughout this program to facilitate the review
process of more complex subject materials in the areas of pathophysiology
and pharmacology. 
Mucosa protecting substances
Antiprotozoal
and Anthelmintic medication
Gastritis
Acute or inflammation of the gastric mucosa by external agents or causes
e. g. NSAID food excess, alcohol excess, caffeine, stress, corticosteroids,
gastroenteritis, gastroesophageal reflux disease (GERD),
autoimmune diseases (Pernicious anemia), bile reflux from biliary system into
the stomach and Helicobacter pylori infection.
Symptoms and diagnostic findings:
Acute or chronic epigastric
pain, aggravating by eating, fetor ex ore, nausea, vomiting, lack of appetite
and bad taste in mouth. Diagnosis in acute
cases is made by physical examination. An endogastroduodenoscopy
is performed in severe or recurrent cases or in cases with recurrent complaints
after treatment.
Treatment:
Treatment of underlying cause.
Medication: Antiemetics, Histamine H2 - antagonists,
Proton pump inhibitors, Mucosal protective agents,
Antacid and Eradication therapy for helicobacter pylori.
Gastroesophageal Reflux Disease GERD
Reflux of stomach content and gastric acids due to a decreased lower
esophageal sphincter tonus. Condition may be caused idiopathic or by a hiatic herniation as well as obesity and external agents e.
g. nicotine, caffeine, fat and fried food, estrogens, anticholinergic drugs,
calcium channel blockers and others.
Long standing GERD leads to a tissue alteration of the inner mucosa from
epithelial into columnal “
Barrett’s epithelium “ cells which can cause esophageal cancer. Cancer
risk increases over time.
Symptoms and diagnostic findings:
Recurrent heartburn, aggravating in supine positions
or while client is bending over as well as in long term fasting conditions or
immediately after a meal.
Long standing GERD may lead to a chronic inflammatory process with
thickening of the esophageal mucosa causing dysphagia, regurgitation and
hoarseness.
Onset of Asthma in adults is commonly associated with GERD.
Main diagnostic evidence is provided by 24h–pH monitoring.
Treatment:
Extinction of causative agents including: Weight management, smoking and
caffeine cessation, upright positioning in bed and small meal nutrition
pattern. Medication: Histamine H2 - antagonists, Proton pump
inhibitors, Mucosal protective agents and Antacids.
Peptic ulcers appear in about 90% of all cases within the duodenum and
in 10% as gastric ulcers. Esophageal peptic ulcers are rare. Duodenal ulcers
are typically caused by an infection with Helicobacter pylori. Gastric ulcers
have the same causes as seen in cases of gastritis but are strongly associated
with NSAID medication which inhibit prostaglandins as
the main acid protecting factor for the gastric mucosa. The severity of a PUD
increases with any coexisting factor that supports a
gastritis as well.
Symptoms and diagnostic findings:
Strong epigastric pain. Pain in duodenal ulcers aggravating especially in
fasting conditions. In comparison to gastritis and gastric ulcers the
intake of food provides pain relief. Helicobacter pylori test positive in >
90% of all cases of duodenal ulcers. In both cases diagnosis is made by EGD
only. Perforation of ulcers can lead to acute peritonitis.
Treatment:
Basic treatment to decrease acid production as in
cases of GERD and Gastritis.
Medication: Histamine H2 - antagonists, Proton pump
inhibitors, Prostaglandin analogons as mucosal
protective agents, Antacids, treatment of a H. pylori infection.
Chronic inflammatory bowel
diseases
The two most common types of chronic inflammatory
bowel diseases are Crohn’s Disease and ulcerative
colitis. Both diseases have in common that they are suspected to be caused by
underlying autoimmune disorders. Other supporting causes like stress and
infections are suspected as well. Both diseases show a chronic recurrent course
and mainly start in young adulthood.
Severity, intensity and recurrence rate vary individually. Extraintestinal manifestations are linked to both types of
IBD, especially arthritis and uveitis. Treatment for both types of IBD is
identical. Corticosteroids in high dosages are prescribed to terminate acute
flares. Depending on the affected intestinal or bowel segments the mode to
administer medication may vary from oral and intravenously to rectal
suppositories. Medication for preventive treatment consists of acetylsalicylic
acid compounds (e. g. sulfasalazine) or immunomodulators
(e. g. azathioprine). Adequate nutrition should consist of a low fiber, high
protein and high calorie diet. The
psychological impact of both conditions is immense since acute flares interfere
strongly with a functioning social life of the affected individual.
·
Crohn’s disease
Crohn’s disease is also described as regional enteritis which mainly affects
the terminal ileum. Although this condition can potentially
affect the entire gastrointestinal tract.
Symptoms and diagnostic findings:
Increased defecation frequency of 5 to 10 stools daily
turning into a semiformed diarrhea.
Severe abdominal cramping mainly in the right lower
abdomen. Fever, weight
loss, body achiness, intraabdominal abscess and
fistulas to other segments of the intestines and bowels and other intraabdominal and intrapelvic
organs. Diagnosis is made by colonoscopy which reveals a typical
“cobblestone” type of lesions which are interrupted by healthy areas of the
mucous membranes, so called “skip lesions”. Histological examination of
biopsies typically reveals granuloma type formations of lymphocytic cells.
Bowel obstruction and rigidity due to a scar tissue development after recurrent
flares is common. Bowel perforations can occur as well but lead mostly to conglomerate
tumors with other bowel segments. Blood examination shows elevated
inflammatory parameters (WBC, ESR, CRP).
Treatment:
Surgical treatment is indicated if medication therapy fails or complications
like bleedings or bowel perforations arise. Surgical treatment of choice is a circumscripted resection of the affected bowel area with a
consecutive end – to end anastomosis of the resection margins. A temporary
Ileostomy may be necessary in cases where the acute inflammation has not come
to a standstill by the time of the surgical intervention.
·
Ulcerative Colitis
Inflammation of the mucosa and submucosa
from rectum over the entire colon. Other parts of the gastrointestinal tract are usually not affected.
Symptoms and diagnostic findings:
Sudden onset of up to 20 diarrheas per 24 hours, even
nocturnal, typically with blood and mucous. Abdominal cramping, fever, weight loss and body
achiness. Flares can cause acute severe intestinal bleedings,
obstructions and perforations.
Treatment:
Surgical treatment is performed as a proctocolectomy
in combination to a temporary ileostomy or colostomy.
Outpouchings of the intestinal wall are considered Diverticula and appear increasingly
by age. Main affected area in 95% of all cases is the sigmoid colon.
Diverticula do not necessarily become symptomatic. Clients with a chronic
constipation tend to retain stool and bacteria within the diverticular pouches.
Symptoms and diagnostic findings:
Classical appearance of an acute diverticulitis is an acute pain in the
lower left quadrant of the abdomen. In accordance to the clinical symptoms this
condition is also called a “left sided appendicitis”. Fever, chills and
increasing abdominal pain are indicating a developing perforation of the
sigmoid colon as the most common complication of diverticulitis.
As in cases of a Crohn’s Disease, a
perforation can also occur “covered”, leading to conglomerate tumors with other
bowel segments and intraabdominal abscedic
infections. Recurrent flares may lead to a fast growth of intraluminal fibrotic
scar tissue which can cause a stenotic condition.
Diagnosis is made by abdominal ultrasound and barium enema.
An ileus describes the situation of an intestinal obstruction and is
usually classified as either a mechanical or nonmechanical
(=paralytic) ileus. Common causes for a mechanical ileus are tumors,
incarcerated and trapped hernias, fibrotic rigidity after intraabdominal
inflammations, adhesions, volvulus or fecal obstructions. A nonmechanical (= paralytic) ileus is caused by a
disturbance of the muscular bowel function, the nerval
bowel innervation or perfusion. Common causes are situations after abdominal
surgery, anesthesia, peritonitis, spinal cord lesions as well as insufficient
blood flow in the mesenterial arteries. A colon ileus
can occur but the most common location is the terminal ileum due to its natural
narrowness.
Symptoms and diagnostic findings:
Abdominal pain, absence of defecation, nausea,
vomiting, alteration of bowel sounds from high pitched to absent, hypotension,
shock due to fluid loss into bowels, signs of peritonitis, elevated
inflammatory parameters, LDH and lactate elevation in blood samples. Diagnosis
is made by x-ray examinations of the abdomen where dilated bowel loops with
fluid entrapment can be seen.
Treatment:
Primary action is the insertion of a nasogastric or nasointestinal
tube to reduce intraintestinal pressure. Fluid
supply, analgesia under restriction of ileus supporting opioid analgesics and
parenteral nutrition. Monitoring of input and output, renal function,
inflammatory parameters, bowel sounds and X-ray’s. Surgical treatment by
partial bowel resection and temporary or permanent ileo
– or colostomy is required if condition is not improving spontaneously or if
complications arise.
The vermiform appendix is the terminal structure of the small intestines
located at the end of the coecum. The appendix is a
lymphoid organ and functionally comparable to tonsils and lymph nodes. Due to
its anatomical configuration it is vulnerable to be obstructed by undigested
food particles, hardened stool or microorganisms which can cause an acute
appendicitis. The local conditions allow this inflammation to develop fast into
an abscess which can potentially cause a life threatening perforation and
peritonitis.
Symptoms and diagnostic findings:
Acute and increasing abdominal pain in the right lower abdominal
quadrant. McBurney – Trigger point, located in the
center of a direct line between the umbilicus and the Crista iliaca anterior superior. Fever, chills, nausea, vomiting
and anorexia. WBC count up to 20000 cell/mm3, elevation of ESR and
CRP.
Treatment:
Acute appendicitis requires immediate appendectomy to avoid or limit a
developing peritonitis. Which is an acute bacterial infection of the peritoneal
cavity. Mostly caused by abdominal wall trauma or rupture of intestinal organs.
Residential bowel bacteria spreading into the blood stream and leading to a
septic shock by release of endotoxins.
·
Celiac disease/Sprue
Gluten sensitive food intolerance syndrome. Affected clients are unable
to digest wheat products containing the proteins gliadine
and gluteine. If condition is present from birth it
is considered Celiac’s disease. A
second form starts during adulthood and is described as Sprue.
Symptoms and diagnostic findings:
After a frequent exposure for several weeks the digestion of gluten
containing products suddenly leads to an acute inflammatory reaction within the
intestinal mucosa. Clients experience massive vomiting and diarrhea of fatty
stool along with severe abdominal cramps. Diagnosis is made by stool analysis
revealing an increased concentration of fat. Duodenal biopsies proof an acute
inflammatory reaction with mucosal damage and degeneration. Antigliadin
and reticulin antibodies are positive in blood
samples.
Treatment:
Clients generally require lifelong gluten – free diet
which is accomplished by a total elimination of any sources of wheat.
·
Lactose intolerance
Caused by a steadily decreasing activity of lactase throughout childhood
and early adolescent age. Clients will remain with a very limited or no lactase
activity and are unable to digest lactase into glucose and galactose.
Treatment requires to maintain a lactose free diet or to substitute oral
lactase prior to indigestion of dairy products. Aged cheeses (e. g. camembert)
and yogurts are mostly tolerated.
The cause of this functional disorder of the gastrointestinal tract is
unknown. Affected clients experience mostly a completely disturbed bowel
function.
Symptoms and diagnostic findings:
Cramping abdominal pain predominantly over the entire lower abdomen.
Unexpected diarrhea and bloatedness especially
shortly after meals.
Constipation also possible. No relevant findings in routine abdominal
diagnostic procedures. Mainly treated as a psychosomatic disorder after other
possible causes are ruled out.
Treatment:
Symptom oriented treatment focuses on high fluid – high fiber diet
regulations, avoidance of stimulating substances (sweets, caffeine and processed food). Symptomatic treatment of
constipation and diarrhea. Psychological support (e. g. Stress Management).
Hereditary and not primarily tumorous, malignant or cancerous
disorder following an autosomal recessive trait. A chromosomal defect on
chromosome 7 leads to non – expression of the cystic fibrosis transmembrane regulator CFTR (a chloride channel). This
results in a disability to move water across cell membranes and disables the Na+Cl- channels as well. As a result
the secretory function of any glandular cell of the body is disabled leading to
a retention of glandular fluids due to thickening which is caused by a lack of
water and chloride within the ICF and an increased chloride concentration in
the ECF. Main symptomatic areas are the respiratory and the digestive tract.
The production of large amounts of thickened mucous within the respiratory
tract leads to occlusion of bronchioles which can not
be cleared by coughing.
Main affected organ in the digestive tract is the pancreatic gland where
essential digestive enzymes can not be discharged
into the duodenum. Deficiency of pancreatic enzymes causes malabsorption
of fats, proteins carbohydrates and fat soluble vitamins. Cystic fibrosis is incurable and usually causes clients to
pass before the age of 40.
Symptoms and diagnostic findings:
Recurrent atypical respiratory infections. Growth
retardation and malnutrition in children and young adults. Prenatal diagnosis
via amniocentesis reveals a reduced intestinal alkaline phosphatase. Meconeum ileus is a common first sign in newborns.
Diagnosis via pilocarpin induced sweat test shows an
increased Cl- concentration of at least
> 60 meq/L. Fatty stools in 72 hour stool sample.
Chest X-rays with signs of mucous infiltrations within the parenchymateous
lung tissue. Clubbing nails as a sign of chronic hypoxemia
Treatment:
Sincere pulmonary hygiene, Postural drainage, specific
antibiotic treatments in cases of bacterial infections. Bronchodilators. High
calorie and high protein diet with prefermentized
ingredients or parenteral supply. Avoidance of exposure to respiratory tract
infections. Frequent physical exercise to increase pulmonary function and
secretion of trapped mucous.
Disorders and Diseases of the
Liver
Hepatitis A
Caused by a fecal - oral droplet infection with Hepatitis A-virus mostly
from contaminated food sources or water in an non-hygienic environment.
Symptoms may start after an incubation period of 15 – 50 days. Infected clients
remain infectious throughout the course of the disease, especially about two
weeks prior to the onset of symptoms.
Symptoms vary from minimal gastrointestinal complaints to a massive
jaundice.
Hepatitis A is usually a self limiting
infection in otherwise healthy individuals. Treatment is oriented on symptoms.
Infection leads to a lifelong immunity against Hepatitis A. Hepatitis A is
vaccine preventable. Acute epidemic infections can be interrupted by mass
treatments with Hepatitis A immunglobuline.
Hepatitis B
Caused by blood borne (= parenteral) infection with DNS containing
Hepatitis B Virus. Infection requires contact between body fluids and occurs
regularly either sexually or by common use of needles amongst intravenous drug
users. Other sources of infection are surgical procedures with contaminated
instruments, blood transfusions and dialysis treatments. Health care workers are
generally endangered by accidential infections as
well. The incubation period is estimated between 30 and 180 days. Clients
remain infectious as long as anti – Hbs is
traceable in blood. 70% of otherwise healthy infected individuals will
experience spontaneous healing within a period of 6 months. About 30% of all
cases will lead to a chronic hepatitis where the virus persists in the liver parenchym, causing a more or less progressive ongoing
hepatitis. In these cases anti – Hbs, anti – Hbe and HBV-DNA remain
as diagnostic markers for the ongoing infection and its activity. Clients with
a chronic persisting hepatitis b have an increased risk for the development of
liver cirrhosis and liver cell carcinoma. The rate of progressive liver
destruction by liver cirrhosis is 20% and 15% for the development of liver cell
carcinoma. In cases of suspected fresh hepatitis b infections it is recommended
to administer hepatitis b vaccine as a postexposure
prophylaxis. A possibly developing chronic hepatitis will be treated with a
combination of interferone and ribavirin for up to 48
weeks depending on the persistence of the infection markers.
Hepatitis C (Hepatitis non–A / non–B)
Hepatitis C is in regards to modes of infection and incubation period
comparable to hepatitis b. Main difference is a comparably much more aggressive
course of infection. 75% of infected individuals develop a chronic hepatitis
with an increased risk for liver cirrhosis and liver cell cancer. Treatment of
a chronic persisting hepatitis c is comparable to the treatment of a chronic
persisting hepatitis b.
Hepatitis D
An infection with Hepatitis D virus requires the presence of a hepatitis
b virus capsule which is needed to allow a proper replication of the hepatitis
d virus. Modes of infection are comparable with hepatitis b. Acute Hepatitis
with a healing rate of 95% can be observed
in cases of a simultaneous infection. Superinfections
in cases of an already developing course of acute hepatitis b lead to a poor
prognosis with high rates of terminal liver failure.
Hepatitis E
Hepatitis E virus infections occur comparable to hepatitis a infections
and show an almost identical outcome. Hepatitis E is currently not endemic in
the United States but in South America, Africa, Asia and the Middle east.
Cirrhosis of the liver
Liver cirrhosis is defined as a stade of
destroyed and dysfunctional liver parenchym and its
replacement by connective fiber tissue. Common causes of liver cirrhosis are
alcoholism, (laennec’s cirrhosis) chronic persisting
hepatitis b and c, biliary diseases, autoimmune hepatitis and metabolic
diseases. Course and severity of liver cirrhosis are determined by the
persisting presence of its cause. Liver cirrhosis is primarily incurable but
its progress can be interrupted or significantly delayed if its cause can be
controlled.
Total liver failure due to a cirrhosis may not occur until 90% of the
organ is affected but multiple complications can derive from a reduced liver
function.
Symptoms and diagnostic findings:
Disturbed protein synthesis and an increased blood
pressure in the portal vein. Physical exhaustion, fatigue, jaundice, pruritus,
weight loss, malnutrition, anorexia and enlarged liver. Delayed blood
coagulation, hematomas, spider angiomata, teleangiectasia, clay colored acholic
stools, altered bowel habits, pleural effusions, breathing difficulties,
immunodeficiency, delayed wound healing, palmar erythema and dark urine.
Umbilical caput medusa, edema, respiratory distress due to sub-diaphragmatical ascites, disturbed menstrual cycle in
women, gynecomastia and erectile dysfunction in men.
Testosterone/Estrogene deficiency.
Pathophysiology of liver failure due to cirrhosis Portal vein hypertension →
Caused by an increased pressure
within the portal vein due to growing resistance caused by fibrotic liver tissue as the most common
cause. Other causes are portal vein thrombosis, liver vein thrombosis (Budd Chiari Syndrome), right sided heart failure. The
increased pressure in the portal vein causes large connecting veins to
expand, leading to the following characteristic symptoms: - Hemorrhoids - Esophageal
and gastric varicosis with potential risk of
hematemesis - Umbilical
vein dilation “caput medusa” - Hepatospenomegaly Ascites → Plasma rich fluid accumulation in the
peritoneal cavity. Caused
by protein deficiency and decreased oncotic pressure.
Aldosterone increase leads to sodium and water retention. Hepatic encephalopathy → Neurological disorder caused by increased ammonia levels due to an
altered hepatic protein metabolism. Symptoms include confusion, altered
consciousness, flapping tremor and disorientation. Hepatorenal
syndrome →
Acute renal failure in
an ongoing and advanced liver failure. Oliguria, hyponatremia and fatigue. Increased creatinine and BUN parameters. Client may
require dialysis to treat fluid excess and hyperkalemia. Liver transplantation
is the only possible cure. Laboratory
findings →
Bilirubin ↑ → Cholinesterase ↓ → Albumin ↓ →
Blood coagulation factors ↓ →
Pancytopenia → Serum ammonia levels ↑, →
Aldosterone level ↑ → Sodium ↓ →
Gamma – globulins ↓ → Fat soluble vitamins ↓ →
Blood Glucose ↓ due to Glycogen deficiency The final diagnosis of a liver cirrhosis always requires liver biopsy which has to be obtained by a blind liver
puncture or laparoscopy!
Ultrasound examinations typically reveal a more or less unevenly shaped
liver surface, diminished liver veins and widened
portal vein.
Treatment:
Treatment is generally focused on resolving underlying causes.
General treatment:
Small frequent meals, anorectic clients require strict prevention of
pressure sores, Monitoring of liver function parameters, Vitamin K supply to
enhance remaining production of coagulation factors and life style change (e.
g. avoiding alcohol).
Ascites treatment:
Paracentesis to drain ascites.
Portal vein bypass by surgical procedure or catheter placement (LeVeen/TIPS)
to treat portal hypertension and avoid recurrence of ascites.
Fluid, sodium and protein restriction.
Daily monitoring of weight, input and output.
Diuretic treatment with Spironolactone and Furosemide
Hepatic encephalopathy treatment:
Lactulose treatment to reduce intestinal ammonium levels produced by
intestinal bacterial flora. Neomycin for bowel sterilization.
Hematemesis treatment:
Intervention in cases of hematemesis from a varicose esophageal bleeding
by sclerotherapy or esophageal tamponade
via Sengstaken – Blakemore or Minnesota tube.
Vasopressin or beta blocker intravenously (under cardiac monitoring) to
cause vasoconstriction of portal vein collaterals.
Gallbladder and biliary duct
disorders
Gall bladder
and biliary duct stones (Cholelithiasis)
Gall bladder and biliary duct stones are the most common disorders of
the biliary system. Gallbladder stones consist in more than 80% of all cases of
cholesterol. The underlying dysfunction for the formation of these stones is
mostly a disproportion between bile salts and the amount of indigested
cholesterol. A deficiency of bile salts can be caused either by their disturbed
hepatic production or inhibited reuptake from the terminal ileum in the
digestion process. A deficit of bile salts leads to limited digestion of fats.
Another possible source for cholesterol stones is a long lasting high
cholesterol diet which can overcome the fat digesting capacity of the
gastrointestinal tract.
Multiple risk factors for the development of gallstones have been described:
Obesity, hyperlipidemia, age > 40 years, caucasian ethnicity, female gender, family history of gall
stones, pregnancy and estrogen supply. Affections and dysfunction of the
terminal ileum (e. g. Crohn’s disease and
tumors),type I diabetes.
Stone formation of pigment stones occurs from a combination of hardened unconjugated bilirubin with
calcium. These stones occur more often within the biliary system, mostly after
a bile duct inflammation (cholangitis) or conditions of increased destruction
of blood cells (e. g. leukemia).
Symptoms and diagnostic findings:
Gallbladder and biliary duct stones can be
asymptomatic for a lifetime. Once a gallbladder got filled with gall stones its
natural function as a reservoir for bile acids is limited or lost which typically
results in digestive problems after fatty or spicy meals as well as larger
amounts of food. A biliary colic occurs if a gallbladder stone moves into the
narrow biliary duct system and gets trapped in there. As a result the affected
client experiences severe fluctuating abdominal pain in the right upper
quadrant. Mostly accompanied by severe nausea and vomiting. Physical examination typically reveals a
sharp pain when client performs deep inspiration while examiner is palpating
the RUQ. (Murphy’s sign) Jaundice,
grey stools, dark urine and elevated bilirubin serum levels occur if colic
leads to a total blockage of the common bile duct. Diagnosis is routinely made via abdominal
ultrasound as well as by abdominal x-rays. Laboratory findings include an
elevation of GPT and GOT as well as GGT and AP as cholestasis indicating
parameters. WBC, ESR and CRP may be altered in cases of a developing
inflammatory process.
Treatment:
Clients with asymptomatic gallbladder stones do not require any curative
treatment. Frequent follow up examinations along with a cholesterol restricted
diet are recommended. Main priority in an acute biliary colic is symptom relief
with common analgesics and spasmolytics. Opiod analgesics are relatively contraindicated since they
increase spasms in smooth muscles.
Symptomatic cholelithiasis usually requires
surgical treatment via cholecystectomy and/ or ERCP (Endoscopic Retrograde Cholangio Pancreticography). ERCP
is commonly indicated in cases of bile duct blockage prior to a cholecystectomy.
Cholecystectomy is usually performed as a minimal invasive laparascopic
transabdominal surgery and requires a clear biliary
passage. Conventional cholecystectomy via laparatomy
may be indicated if a larger part of the biliary duct system has suffered
damage from a colic or if biliary stones can not be
captured via ERCP. In these cases surgery involves temporary placement of a
T–Drain which leads biliary fluids through the abdominal wall until the biliary
system has healed. Drain will be removed when bile flow subsides. Flow should
not over exceed 500 mL within the first 24 hours and should gradually decrease
in the following days. Other forms of treatment are Extracorporal
Shock Wave Lithotripsy (ESWL). Oral Ursodesoxycholic
acid (UDCA) to dissolve gall stones of less than 2cm in diameter. Treatment
lasts up to several years. High recurrence rates.
Cholecystitis
An acute or chronic inflammation of the gall bladder. Mostly of lithogenic cause due to an obstruction of the cystic duct
or the common bile duct due to an inhibited flow of biliary and pancreatic
fluids as well as other digestive enzymes. Other causes are a previous
gallbladder or biliary duct surgery as well as a vast overproduction of biliary
fluids in cases of hyperalimentation with fats.
Symptoms and diagnostic findings:
Symptoms of an acute cholecystitis mostly
occur during an acute biliary colic and show comparable symptoms. Advanced
inflammations can lead to peritonitis. Laboratory findings are irregular liver
function tests, especially elevated cholestasis parameters and inflammatory
parameters. Abdominal ultrasound examination reveals an edematous gall bladder
wall. Proof of inflammation in chronic stades via
nuclear scans. (HIDA– Hepatobiliary Imino Diacetic Acid).
Treatment:
Acute inflammation needs to be cured prior to any surgical treatment of
underlying cause! Clients remain in NPO status under intravenous antibiotic
treatment and analgetic medication until acute
infection is under control. Emergency cholecystectomy may become necessary in
case of peritonitis.
Primary Sclerosing
Cholangitis (PSC)
Incurable autoimmune inflammatory process which leads to a progressive
destruction of the entire biliary system.
Symptoms and diagnostic findings:
Repeated cholestasis, jaundice, abdominal pain in upper right quadrant
and anorexia.
Proof of diagnosis via assessment of pANCA
antinuclear antibodies. Otherwise elevated GGT, AP and inflammatory parameters.
Progress leads to biliary cirrhosis of liver. Up to 10% of affected individuals
experience cholangiocarcinoma or colorectal cancer.
Diagnosis is made by liver biopsy.
Treatment:
Symptom oriented treatment of cholestatic
episodes including dilating procedures of biliary ducts. Only curative
treatment is liver transplantation.
Increased amount of pancreatic enzymes in pancreatic duct leads to
pancreatic inflammation and autodigestion.
Inflammatory swelling of pancreatic duct occludes
Sphincter oddi and ampulla Vateri
and inhibits flow. Hemorrhagic organ destruction may lead to retroperitoneal
hematoma.
Major causes of pancreatitis are:
Obstructive biliary stones leading to a reflux of digestive pancreatic
enzymes.
Alcohol and alimentary excess causing hypertriglyceridemia with an
increased production of pancreatic enzymes lipase and amylase. Rare causes are
side effects of medication e. g. NSAID, Thiazides and abdominal traumas.
Symptoms and diagnostic findings:
Acute epigastric abdominal pain and
tenderness, increasing in supine position,
Hematoma in both flanks and/or around umbilicus (Grey
– Turner sign/Cullen sign).
Hemorrhagic ascites, pleural effusions, hypovolemia
and shock. Also nausea, vomiting, diarrhea and fever. Abdominal ultrasound and
CT–scans reveal inflammatory pancreatic edemas and bleedings, gall and biliary
duct stones, ascites and pleural effusions.
Laboratory findings: Blood Glucose, Lipase, Amylase ↑↑,
Urine Amylase↑, Hypocalcemia, CRP and
Leucocytes ↑↑.
Recurrent episodes of acute pancreatitis may lead to chronic pancreatitis
with a resulting exocrine pancreatic insufficiency. Main symptom is a food
intolerance against fat.
Treatment:
Depending on the severity of an acute pancreatitis
treatment includes, pain relief, antibiotic treatment, antispasmodic treatment,
nasogastric tube to drain excess digestive fluids, parenteral nutrition,
correction of hyperglycemia, adjustment of electrolyte status and fluid supply.
Curative treatment of underlying cholelithiasis is
performed after acute episode of pancreatitis is controlled.
GASTROINTESTINAL MEDICATION THERAPY
Antispasmodics
Pharmacological effect:
Antagonizing effect on the acetylcholine receptors of the smooth muscles
of the gastrointestinal tract.
Therapeutic effect:
Relaxation of smooth muscles to increase gastrointestinal motility.
Indications:
Gastrointestinal dysfunction, cramping, pylorospasms and inflammatory bowel disease.
Special considerations: Medication should be taken
about 30–60 min. prior mealtimes.
Side effects:
Dry mouth, nausea, vomiting, constipation, mydriasis,,
urine retention, impotence, tachycardia, palpitations, dysphagia, hyperthermia
due to inactivity of sweat glands, allergic rash and urticaria.
Substances:
Hyoscyamine sulfate (Levsin®), Dicyclomine
hydrochloride (Bentyl®), Chlordiazepoxide
hydrochloride (Librax®) and Glycopyrrolate
(Robinul®).
Pharmacological effect:
Reduction of bowel motility by interaction with
intestinal motoric nerves.
Therapeutic effect:
Diarrhea relief
Indications:
Diarrhea
Special considerations:
Self treatment with OTC Medications is tolerable for 2 days in a case of diarrhea.
Main concern is the development of dehydration, especially in elderly or
pediatric clients. Adequate fluid supply and an easy digestible diet. (i. e. BRAT
Diet = Banana, rice, applesauce, tea, toast is also a part of the
treatment) Dairy products aggravate diarrhea. Pregnant and lactating women
need to seek medical attention early!
Contraindications:
Bloody diarrhea, bacteria induced Diarrhea (E. Coli
and Shigella), bowel obstruction.
Difenoxine: Not indicated for children < 2 years and in combination with MAOI
medication.
Substances:
Loperamide (Imodium®)
Categories:
·
Stimulant laxatives
·
Bulk forming
laxatives
·
Stool softeners
·
Hyperosmotic
laxatives
·
Lubricants
·
Saline Laxatives
Laxatives are indicated in the treatment of constipation only. The
individual pattern on how often a human being defecates can differ widely between
individuals. Therefore the individual regularity of bowel movements is of
greater importance for judging about a constipation than the actual frequency.
An exception from this rule is the abrupt and ongoing alteration of bowel
habits which should always be further investigated since this could indicate a
suspicion of bowel cancer or another intestinal or systemic disease.
The main factors which regulate a normal bowel
function are a fiber rich diet, daily
physical activity and sufficient amount of fluids. Therefore
constipation is of great concern for clients who are lacking sufficient
mobility. A constipation also may occur as a side effect of certain medications
and is most common for opioid analgesics of all potencies. Long term use of
laxative and laxative abuse weakens the muscular bowel function and can lead
into a state of bowel immobility due to a chronic ulcerative colitis. A general
contraindication for laxatives are any mechanical bowel obstructions i. e. due
to a tumorous or inflammatory or stenosis. Administration of laxative agents
should take place separately from any other medication.
Stimulant laxatives
Pharmacological effect:
Stimulation of parasympathic bowel innervation
due to mucosa irritation.
Special considerations:
Effect to be expected 6–12 hours after oral administration and within 2
hours after rectal administration. Not to be taken with milk or antacids.
Contraindications:
Abdominal colicky pain, nausea, vomiting, rectal bleeding,
gastroenteritis and intestinal obstruction. Castor oil can cause premature
labor.
Senna is excreted in breast milk.
Side effects:
Hypokalemia, hypocalcemia,
abdominal cramping and colicky pain.
Substances:
Bisacodyl (Dulcolax®), Castor oil (Neoloid®,
Purgo®), Senna (Senokot®) and Casanthranol (Pericolace®)
Bulk forming laxatives
Pharmacological effect:
Non-absorbable polysaccharide molecules increase in size by binding
water. The resulting bulk formation is distending the colon wall as an adequate
trigger to release peristaltic action.
Special considerations:
Slow onset of effect within 12 hours to 3 days. Strictly requires
sufficient fluid supply! Pat is otherwise endangered of bulk forming process in
upper gastrointestinal tract.
Substances:
Calcium polycarbophil (Fibercon®),
Methylcellulose (Citrucel®) and Psyllium (Metamucil®)
Hyperosmotic laxatives
Pharmaceutical effect :
Equivalent to bulk forming laxatives, orally or rectally administered
disaccharides absorb water which leads to a softening effect without bulk
formation.
Special considerations:
Onset of effect may be delayed by 2 – 4 days.
Substances:
Lactulose (Kristalose®), Polyethylene glycol (Miralax®) and Glycerine
(Glycerol®)
Stool softeners (emollient laxatives)
Pharmaceutical effect:
Anionic surfactants diluted in water penetrate into
dry formations of stool.
Special considerations:
Effect is delayed by up to 3 days from first dosage. Main indication is
the prevention of strainous defecation in clients at
special risk for constipation (i. e. elderly and immobile clients with limited
fluid intake).
Substances:
Docusate sodium (Colace®), Docusate potassium (Dialose®) and Docusate calcium (Doxidan®)
Saline Laxatives
Pharmacological effect:
Non-absorbable Magnesium
sulfate or citrate salts or Sodium phosphate salts lead to a fast defecation.
Special considerations:
Onset of effect between 30 Minutes and 6 hours after
administration.
Side effects:
These laxatives may get partially absorbed.
(Relative)Contraindications:
Renal impairment:
Magnesium salts.
Chronic heart failure: Sodium salts
Antihistamines
Most commonly used for treatment of motion sickness. Antiemetic effect
due to anticholinergic side effect.
Substances:
Cyclizine HCl (Marezine®), Dimenhydrinate (Dramamine®), Diphenhydramine (Benadryl®),
Hydroxyzine (Vistaril®) and Meclizine (Antivert®).
Phenothiazines and Butyrophenone:
Antiemetic effect due to dopamine receptor blockade.
Substances:
Metoclopramide (Reglan®), Perphenazine (Phenazine®), Prochlorperazine
(Compazine®) and Promethazine HCl (Phernergan®).
Cannabinoids
Mechanism unknown. Used as an antiemetic in cancer
chemotherapy.
Substances:
Dronabinol (Marinol®) and Nabilone
(Cesamet®)
(also used in AIDS treatment for appetite enhancement)
Benzodiazepines and Glucocorticoids
Antiemetics in cancer chemotherapy. Used in combination along with Metoclopramide.
Substances:
Diazepam (Valium®) and Lorazepam (Ativan®)
Serotoninantagonists
Antiemetic effect is part of the Serotonin antagonism.
Substances:
Dolasetron mesylate
(Anzemet®), Granisetron (Kytril®), Ondansetron (Zofran®), Palonosetron (Aloxi®)
H2 Histamine Blockers
Pharmacological effect:
Selective blockage of H2 - Receptors in
gastric, duodenal and pancreatic secretory cells.
Reduction of acid release in gastric, duodenal and
external pancreatic cells. Peptic ulcer disease, reflux esophagitis and Zollinger-Ellison’s syndrome.
Physiological effect:
Reduction of gastric acid production.
Special considerations :
Reduced dosages in hepatic or renal impairment. Successful treatment
requires dietary and life-style regulations. Normal oral dosage is administered
once daily at bedtime. NSAID and ASA may interfere with therapeutic effect.
Side effects:
Dysrhythmias and blood dyscrasias.
Substances:
Cimetidine (Tagamet®), Famotidine (Pepcid®), Ranitidine (Zantac®) and Nizatidine (Axid®)
Protone pump inhibitors
Pharmacological effect:
Blockage of acid producing gastric parietal cells by inhibiting H+-K+
ATPase and removing protons from acid building process.
Physiological effect:
Reduction/elimination of gastric acid.
Indication:
GERD, gastric and duodenal ulcers.
Special considerations:
Used for long–and short term treatment depending on underlying
conditions. Lansoprazole and Esomeprazole capsules
can be crushed and administered pellet wise. Omeprazole, Rabeprazole
and Pantoprazole capsules can not be opened.
Medication has to provide full symptom relief. Otherwise dosage increase or
change of medication is required. Intravenous administration has to be
performed slow over 15 minutes. Requires reduced dosage in case of a liver
impairment. Ongoing Assessment of laboratory parameters is mandatory.
Contraindications:
Children, pregnancy and lactating women.
Side effects:
Disturbed digestion due to absence of gastric acid, resulting in nausea,
flatulence, constipation, diarrhea, increased liver enzymes, hepatic failure,
liver necrosis, toxic epidermal necrolysis, Stevens
Johnson Syndrome and Agranulocytosis.
Substances:
Pantoprazole (Protonix®), Esomeprazole (Nexium®), Lansoprazole (Prevacid®)
Rabeprazole (Aciphex®) and Omeprazole (Prilosec®).
Pantoprazole (Protonix®), Esomeprazole (Nexium®), Lansoprazole (Prevacid®)
Misoprostol (Prostaglandine)
Pharmacological effect:
Prostaglandine effect on gastroduodenal
mucosa cells: ·
Inhibition of gastric secretion, ·
increase of gastric bicarbonate, ·
increase of mucus production ·
decrease of pepsin cells.
Physiological effect:
Gastric acid relief and mucosa protection.
Indications:
Mucosa protection
Special considerations:
Misoprostol has to be taken with food. Strict contraception under Misoprostol
is required for up to 1 month after treatment has ended.
Side effects:
Dizziness, nausea, vomiting, laryngospasm, seizures,
dysmenorrhea and postmenopausal
bleeding.
Sucralfat
Pharmacological effect:
Formation of a pepsin absorbing coating from albumin and fibrinogen on
an gastroduodenal ulcer site.
Physiological effect:
Gastroduodenal ulcer protection.
Indications:
Gastrodudenal ulcers
Special considerations:
Medication to be taken 1 hour prior or 2 hours after
meals and 2 hours after medication.
Antacid medication
Pharmacological effect:
Anionic magnesium and aluminum molecules to neutralize
gastric acids.
Therapeutic effect:
Gastric acid relief.
Specific considerations:
Used for symptom oriented treatment on demand only.
Magnesium has to be used cautiously in cases of renal impairment !
Side effects:
Magnesium may cause diarrhea, aluminum may cause constipation and
hypophosphatemia.
Contraindications:
Lactating women.
Magnesium: Severe renal impairment, Ileostomy,
Colostomy.
Substances:
Magnesium trisilicate (Gaviscon®),
Magnesium hydroxide and aluminum hydroxide (Maalox®) and Calcium carbonate
(Tums®).
Helicobacter pylori treatment schemes Lansoprazole + Amoxicillin + Clarithromycin (Prepak®) most effective! Bismuth
salicylate + Metronidazol + Tetracycline (Helidac®) Omeprazole
+ Clarithromycin (Prilosec/Biaxin®) Ranitidine + Bismuth citrate + Clarithromycin (Titrec/Biaxin®) Special considerations : Course has to be completed
within one week. Clarithromycin and bismuth can not be administered to pregnant women! Bismuth is contraindicated in
children (Danger of Reye-Syndrome) and
may change color of tongue and stool.
Pharmacological effect:
Bile acid, inhibiting hepatic synthesis and secretion
of cholesterol.
Therapeutic effect:
Removal of gall stones.
Indication:
Gallbladder stones
Special considerations:
Treatment requires 12–24 months and must show gradual improvement in 6
monthly frequent ultrasound investigations to be continued.
Side effects:
Rash, nausea, vomiting, abdominal pain, photosensitivity and anxiety.
Contraindications:
Calcified stones, obstruction of biliary system and
liver disease.
Substances:
Urosodiol (Actigall®)
Pharmacological effect:
Replacement of pancreatic enzymes lipase, amylase and
protease.
Therapeutic effect:
Restoration of excretoric
pancreatic function.
Indication:
Chronic pancreatitis
Special considerations:
Medication has to be linked to meals. No combination with other
substances.
Side effects:
Nausea, diarrhea and hyperuricemia.
Substances:
Pancrease and Viokase (Creon 5®)
Therapeutic effects:
Treatment and prevention of Gardiasis,
Threadwom infections, Cestodiosis
and
Malaria
infections.
Special considerations:
Quinacrine:
Used for treatment of tapeworm giardiasis and cestodiosis.
As a sclerosing agent for injection into the pleural
space used to prevent recurrence of pneumothorax. To be taken after food.
Substance may cause reversible yellow blueish
coloration of ears, nasal cartilage and nail beds.
Chloroquine:
Used for giardiasis and amebiasis treatment.
To be taken with food. Prophylactic treatment once weekly during current risk
and for 10 weeks afterwards. May cause bleaching of body and scalphair, bluish black skin coloration, rusty yellow or
brown urine and photophobia.
Side effects:
Decreased visual acuity, dizziness, vertigo, headaches,
nausea, vomiting, diarrhea, confusion, delirium, insomnia, cardiotoxicity,
bone marrow suppression, hypotension, blackwater
fever and interaction with anticonvulsive agents.
Commonly used substances:
Chloroquine (Aalen®), Mefloquine (Lariam®),
Primaquine, Pyrimethamine (Daraprim®)
Quinacrine (Atabrine®), Quinine sulfate (Quinamm®), Pentamidine isethionate (Pentem 300®)
Pneumocystis carinii infection.
Anthelmintic Medication
Treatment of infection with Ascaris
lumbricoides, trichostrongylus,
enterobius vermicularis, ancystoma duodenale and necator americanus.
Commonly used substances:
Mebendazole (Vermox®), Piperazone
(Antepar®), Pyrantel pamoate (Antiminth®), Thiabendazole (Mintezol®)
END OF CHAPTER
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