NCM116GEP MIDTERMS
• MRI
GASTROINTESTINAL TRACT DISORDERS
Alimentary Canal
• The gastrointestinal tract is a 23- to 26-foot-long (7m to
7.9m) pathway that extends from the mouth to the
esophagus, stomach, small and large intestines, and
rectum to the terminal structure, the anus.
Function:
• Digestion
• Absorption
• Elimination
CONTROL OF GASTROINTESTINAL MOTILITY
• Peristalsis - coordinated sequential contraction and
relaxation of smooth muscles
• Rhythmic Movements - intermittent contractions that
are responsible for mixing and moving food along the
digestive tract
• Tonic Movements - consist of a constant level
contraction without periods of relaxation ; found in the
lower esophagus, upper region of the stomach,
ileocecal valve and internal anal sphincter
GASTROINTESTINAL SECRETIONS
Secretory glands serve two basic functions:
• production of mucus to lubricate and protect the
mucosal layer of the GI tract wall
• secretion of fluids and enzymes to aid in the digestion
and absorption of nutrients.
COMMON MANIFESTATIONS OF GIT DISORDERS:
• Abdominal pain
• Anorexia – lack of desire to eat despite physiologic
stimuli that would normally produce hunger
• Dyspepsia – upper abdominal discomfort from
indigestion with pain, discomfort, fullness, bloating,
early satiety, belching, heartburn or regurgitation
• Intestinal gas – accumulation of gas in the GIT resulting
in belching and flatulence
• Nausea and vomiting
• Change in bowel habits:
→ diarrhea, constipation, fecal incontinence
• Changes in stool color and characteristics:
→ melena (black-tarry stool secondary to upper GI
bleeding)
→ hematochezia (bright or dark red stool secondary
to lower GI bleeding)
→ steatorrhea (greasy and fatty stool)
COMMON DIAGNOSTIC TESTS FOR GIT DISORDERS:
Serum Laboratory tests – triglycerides, liver function tests
• CEA – Carcinoembryonic Antigen
• CA – Cancer Antigen
Stool tests – fecal fat, pathogens, parasites
• FOBT – Fecal Occult Blood Testing to check for occult
(hidden) blood
Abdominal ultrasonography
Imaging studies
• Abdominal X-ray
• CT-scan
• Upper GIT study / Barium Swallow – a radiopaque
liquid contrast agent (barium sulfate) is used to detect
or exclude anatomic or functional disorders of the
upper GI organs or sphincters.
→ May be extended to examine the duodenum (to
check for gastric emptying)
→ Multiple x-ray films are obtained during the
procedure
→ Clear liquid diet then NPO after midnight
→ Increase oral fluid intake to facilitate
evacuation of stool and barium
• Lower GIT study / Barium Enema – visualization using
x-ray images of the lower GIT after rectal installation of
barium used to determine anatomic abnormalities or
malfunctioning of the bowel.
→ Low residue diet 1 to 2 days before the test
→ Clear liquid or laxative the evening before the
procedure
→ NPO after midnight
→ Cleansing enema
→ Make sure that lower GI studies are performed
first prior to upper GI studies
→ Increase oral fluid intake to facilitate
evacuation of barium, expect more bowel
movements
Imaging Studies: Endoscopic procedures
• Esophagogastroduodenoscopy (EGD) / Upper
Gastrointestinal Fibroscopy – Direct visualization of
the esophageal, gastric and duodenal mucosa using
a lighted endoscope
→ NPO for 8 hours prior to the examination
→ Local anesthetic gargle/spray is administered
→ Sedatives to relieve anxiety
→ Atropine sulfate to reduce secretions
→ Left lateral position to clear secretions and
facilitate smooth entry of the endoscope
• Colonoscopy – Direct visualization of the bowel
→ Colon cleansing: cleansing enema, fleet enema,
laxatives, NPO after midnight, clear liquids and
light meals the night before the procedure
→ Colonoscopy cannot be performed when there is
suspected or documented colon perforation
→ Sedatives to relieve anxiety
 NCM116GEP MIDTERMS

ESOPHAGUS DISORDERS
ESOPHAGUS
• The esophagus (25 cm or 10 in) is located in the
mediastinum anterior to the spine and posterior to the
trachea and heart.
• Passageway of food from the mouth to the stomach.
Sphincters:
→ Upper Esophageal Sphincter
→ Lower Esophageal Sphincter – cardiac sphincter

DISORDERS OF THE ESOPHAGUS

GASTROESOPHAGEAL REFLUX DISEASE (GERD)
• backflow of gastric or duodenal contents into the
esophagus
• Etiology: incompetent lower esophageal sphincter,
pyloric stenosis, motility disorder, hiatal hernia,
gastric or duodenal ulcers

CLINICAL MANIFESTATIONS
• Pyrosis – burning sensation in the esophagus
(heartburn)
• Dysphagia – difficulty in swallowing
• Dyspepsia – indigestion
• Upper abdominal pain within 1 hour after eating
• Hypersalivation – sialorrhea or ptyalism
• Esophagitis – inflammation of the esophagus

DIAGNOSTICS
• Endoscopy – Esophagogastroduodenoscopy
• Barium swallow

MANAGEMENT
• Low fat diet, avoid caffeine, tobacco, beer, milk, foods
with mint, carbonated beverages
• Avoid eating 2 hours before bedtime
• Main normal body weight
• Elevate head of bed or upper body on pillows
• H2 receptor antagonists – ranitidine
• Proton pump inhibitors – omeprazole
• Prokinetic agents – accelerates gastric emptying –
domperidone, metoclopramide
• Surgery: Nissen fundoplication – wrapping of a
portion of the gastric fundus around the sphincter
area of the esophagus
 NCM116GEP MIDTERMS
• Dietary and lifestyle modifications: nonirritating diet,
STOMACH DISORDERS refrain from smoking, caffeine, alcohol and NSAIDs
STOMACH • Monitor for signs of hemorrhagic gastritis:
• Average capacity: 1500 ml hematemesis, tachycardia and hypotension
• Stores food during eating, secretes digestive fluids, • Antibiotic therapy for H. pylori infection
and propels the partially digested food, or chyme, into
the small intestine. PEPTIC ULCER DISEASE (PUD)
• Gastric secretions – for digesting food and destruction • An excavation (hollowed-out area) that forms in the
of bacteria mucosal wall that may extend as deeply as the muscle
• Parietal cells – secrete HCl layers or through the muscle to the peritoneum.
Sphincters: • Gastric (pylorus) ulcer
• Pyloric sphincter – gastric sphincter; junction • Other locations: Duodenal ulcer, Esophageal ulcer
between stomach and duodenum • Etiology: Helicobacter pylori infection, excessive HCl
secretion (may be caused by milk, caffeine, alcohol,
DISORDERS OF THE STOMACH smoking, spicy food), Zollinger-Ellison syndrome
GASTRITIS
Inflammation of the stomach mucosa CLINICAL MANIFESTATIONS
Etiology: • Dull gnawing pain or burning sensation in the mid-
• Acute gastritis: eating irritating or contaminated food, epigastrium or the back
overuse of NSAIDs such as aspirin, excessive alcohol • Pyrosis (heartburn)
intake, bile reflux, radiation therapy, ingestion of • Nausea and vomiting
strong acid or alkali. • Belching and sour taste
• Chronic gastritis: benign or malignant ulcers of the • Bleeding: hematemesis or melena
stomach, Helicobacter pylori infection, excessive
alcohol intake, smoking, chronic reflux of pancreatic DIAGNOSTICS
secretions and bile into the stomach.
• Esophagogastroduodenoscopy (EGD)
• Barium study of upper GI tract
CLINICAL MANIFESTATIONS
• Fecal occult blood testing
• Abdominal discomfort
• Biopsy of gastric mucosa through endoscopy
• Heartburn
• Rapid urease test using the biopsy specimen
• Anorexia, nausea and vomiting
• Possible gastric bleeding
MANAGEMENT
• Hiccupping lasting from few hours to few days
• Antibiotic therapy for H. pylori infection
• Belching
• H2 receptor antagonists and proton pump inhibitors
• Sour taste in the mouth
• Reducing environmental stress requires physical and
• Achlorhydria / Hypochlorhydria - absence or low psychological modifications
levels of HCl
• Smoking cessation
• Hyperchlorhydria - high levels of HCl • Dietary modifications: avoid milk, caffeine, alcohol
and have 3 regular meals a day
DIAGNOSTICS
• Small frequent feedings may not be necessary as long
• Esophagogastroduodenoscopy (EGD)
as antacids are taken.
• Upper GI X-ray studies
• Biopsy: histologic examination of tissue specimen
• Rapid urease test using the biopsy specimen

MANAGEMENT
• Antacids to neutralize strong acids (aluminum
hydroxide)
• Diluted lemon juice or vinegar to neutralize strong
alkali
• Emetics and lavage are avoided if extensive corrosion
is present
• Analgesics
• Sedatives MANAGEMENT
• Nasogastric intubation may be necessary Surgery
• Reducing stress → recommended only when ulcers fail to heal after 12
• Surgery: removal of gangrenous or perforated tissue to 16 weeks with medical treatment or with life-
threatening hemorrhage, perforation or obstruction
• Gastric resection or gastrojejunostomy: anastomosis
of jejunum to the stomach to detour around the • Vagotomy – severing of the vagus nerve to reduce
pylorus may be necessary to treat pyloric obstruction gastric acid secretion
 NCM116GEP MIDTERMS
• Pyloroplasty – longitudinal incision is made into the
pylorus and transversely sutured to enlarge the outlet
and relax the muscle
• Gastroduodenostomy (Billroth I) – removal of the
pyloric antrum portion of the stomach and
anastomosed with the duodenum
• Gastrojejunostomy (Billroth II) – removal of the pyloric
antrum portion of the stomach and anastomosed with
the jejunum
 NCM116GEP MIDTERMS
INTESTINE DISORDERS
SMALL INTESTINE
• The longest segment of the GI tract (7000 cm or 70m
of surface area for secretion and absorption through
which nutrients enter the bloodstream through the
intestinal walls)
• Segmentation contractions – produce mixing waves
that move the intestinal contents back and forth in a
churning motion
• Intestinal peristalsis – propels the contents of the
small intestine toward the colon
Sphincters:
• Ileocecal valve
LARGE INTESTINE
• Also known as colon and functions in drying out
indigestible food residue by absorbing water prior to
elimination (150cm or 5 feet)
• Bacteria – major component of the contents of the
large intestine, assist in completing the breakdown of
waste material, especially of undigested or
unabsorbed proteins and bile salts.
• Mass movements - Intermittent strong peristaltic
waves propel the contents for considerable
distances initiating defecation.
Sphincters:
• Internal anal sphincter – autonomic nervous control
• External anal sphincter – cerebral cortex control
DISORDERS OF THE SMALL & LARGE INTESTINE
IRRITABLE BOWEL SYNDROME (IBS)
• is a functional gastrointestinal disorder characterized
by a variable combination of chronic and recurrent
intestinal symptoms not explained by structural or
biochemical abnormalities.
• Etiology is uncertain but the following are considered
based on increasing evidence:
• Infections or inflammatory disorders
vascular/metabolic disturbances or genetic related
changes lead to neuroendocrine dysregulation
(bidirectional brain-gut-axis)
• Psychosocial factors including early life trauma or
abuse or emotional stress interacting with
neuroendocrine, neuroimmune, autonomic nervous
system, and pain modulatory responses
• Alterations in gut microbiota and food antigens may
activate the mucosal immune system and
hypersensitivity reactions, interacting with higher
brain centers
CLINICAL MANIFESTATIONS
• Recurrent abdominal pain and discomfort
• Abdominal bloating and flatulence
• Anorexia and nausea
• Altered bowel habits: constipation or diarrhea
DIAGNOSTICS
• Stool examinations
• Contrast x-ray studies
• Colonoscopy and barium enema may be performed to
rule out other colon diseases
MANAGEMENT
• Pain management
• Controlling diarrhea of constipation
• Restriction and gradual reintroduction of foods that are
possibly irritating may help determine what type of food
are acting as irritants.
• Exercise can assist in reducing stress, anxiety and
increasing intestinal motility
APPENDICITIS
• Inflammation of the appendix, which is a small
fingerlike appendage about 10 cm long attached to the
cecum.
• Etiology: obstruction (fecalith – hardened mass of
stool, tumor or foreign body)
• The appendix fills with food and empties regularly into
the cecum. Because it empties inefficiently and its
lumen is small, the appendix is prone to obstruction and
is particularly vulnerable to infection
CLINICAL MANIFESTATIONS
• Vague epigastric or periumbilical pain (dull and poorly
localized) and progresses to right lower quadrant pain
(sharp, discrete and well localized)
• Low grade fever
• Nausea and vomiting
• Loss of appetite
• Abdominal distention secondary to paralytic ileus
• Local tenderness at the McBurney’s point when
pressure is applied
• Positive Blumberg’s sign
• Positive Psoas sign
• Positive Rovsing’s sign
• Positive Obturator sign
or
COMPLICATIONS
→ Peritonitis secondary to perforation of the appendix
→ Abscess formation (collection of purulent material)
→ Portal pylephlebitis an uncommon thrombophlebitis
of the portal vein or any of its branches that is caused
by infection
DIAGNOSTICS
• Elevated WBC and neutrophils in CBC
• Abdominal x-rays
• Ultrasonography
• CT-scans
MANAGEMENT
• Appendectomy – surgical removal of the appendix
• Immediate surgery is required to decrease the risk of
perforation or rupture appendix.
• Antibiotic therapy – for ruptured appendicitis –
peritonitis and attachment of drains to evacuate the
abscess
• Pain management
 NCM116GEP MIDTERMS
• Monitoring of intestinal obstruction, secondary
hemorrhage and secondary abscess if the appendix PERITONITIS
ruptured leading to peritonitis • Inflammation of the peritoneum, the serous membrane
lining the abdominal cavity and covering the viscera.
DIVERTICULAR DISEASE • Etiology: bacterial infection – organisms from the GI
• A diverticulum is a saclike herniation of the lining of the tract or from internal reproductive organs in women,
bowel that extends through a defect in the muscle layer. injury or trauma, ruptured appendicitis, perforated
• Diverticulosis exists when multiple diverticula are diverticulum, perforated ulcer, bowel perforation,
present without inflammation or symptoms. tumor perforation
• Diverticulitis results when food and bacteria retained in
a diverticulum produce infection and inflammation that CLINICAL MANIFESTATIONS
can impede drainage and lead to perforation or abscess • Abdominal pain aggravated by movement
formation. • Abdominal tenderness and distention
• Etiology: increased intracolonic pressure, lack of fiber • Abdominal muscle rigidity
in the diet, decrease in physical activity, and poor bowel • Anorexia, nausea and vomiting
habits (neglecting the urge to defecate), aging process • Paralytic ileus
• Ascites
CLINICAL MANIFESTATIONS • Fever
Diverticulosis • Tachycardia, Hypotension
• Bowel irregularities with intervals of diarrhea
• Nausea and anorexia COMPLICATIONS
• Bloating and abdominal distention • Septicemia
• Abdominal cramps and constipation • Shock and hypovolemia
• Bowel adhesions leading to intestinal obstruction
Diverticulitis
• Mild to severe pain in left lower quadrant DIAGNOSTICS
• Anorexia, nausea and vomiting • WBC count
• Fever and chills • Serum sodium and potassium
• Leukocytosis • Imaging studies: abdominal x-ray, CT-scans, MRI
• Fatigue and weakness • Ultrasonography
• Peritoneal aspiration and culture and sensitivity
COMPLICATIONS
→ Abscess formation MANAGEMENT
→ Fistula (abnormal tract) formation • Fluid and electrolyte replacement
→ Obstruction • Pain management: analgesics
→ Perforation • Antiemetics for nausea and vomiting
→ Peritonitis • Gastrointestinal intubation and suction
→ Hemorrhage • Oxygen therapy
• Intubation and ventilatory assistance may be required
DIAGNOSTICS
if peritonitis leads to septic shock
• Colonoscopy with biopsy to rule out other diseases • Antibiotic therapy
• Barium enema • Surgical removal of the infected material and
• Abdominal x-rays and CT scan with contrast correcting the cause
• Excision - appendix
MANAGEMENT
• Resection with or without anastomosis – intestines
• Dietary modifications: high-fiber and low-fat diet
• Repair – perforation
• Medications: analgesics, antispasmodics, laxatives,
• Drainage – abscess
antibiotics
• Surgical intervention is necessary if complications like INFLAMMATORY BOWEL DISEASE
perforation, peritonitis, hemorrhage and obstruction
2 chronic inflammatory GI disorders:
occur
→ Crohn’s Disease
Surgery
→ Ulcerative Colitis
• One-stage resection – the inflamed area is removed and
• Etiology: unknown but may be triggered by
a primary end-to-end anastomosis is completed
environmental agents such as pesticides, food
• Multiple-stage procedures for complications such as
additives, tobacco, radiation, NSAIDs; gene
obstruction and perforation
susceptibility; alterations in epithelial cell barrier
→ A two-stage resection may be performed in which
functions, altered immune response to intestinal
the diseased colon is resected but no anastomosis microflora
is performed. A colostomy is constructed instead.
 NCM116GEP MIDTERMS

CROHN’S DISEASE DIAGNOSTICS

• chronic (prolonged) inflammation of the GI tract wall • Stool examination – occult blood or parasite check
that extends through all layers. • CBC: hematocrit, hemoglobin, WBC levels
• commonly occurs in the distal ileum and ascending • Serum electrolytes
colon. • Ultrasonography
• Abdominal x-rays, CT-scans, MRI
CLINICAL MANIFESTATIONS • Colonoscopy
• Right lower quadrant abdominal pain • Barium enema
• Abdominal tenderness and spasm
• Weight loss, malnutrition and secondary anemia (lack MANAGEMENT
of iron in the diet) • Nutritional therapy: oral fluids and low-residue, high-
• Intestinal ulcers with edema protein, high-calorie diet with supplemental vitamin
• Diarrhea, fluid loss and steatorrhea secondary to therapy and iron replacement.
disrupted absorption • IV therapy for dehydration and electrolyte replacement
• Fever and leukocytosis for imbalances
• Pharmacologic management:
COMPLICATIONS → Aminosalicylates (anti-inflammatory drug) –
• Perforation secondary to inflammation sulfasalazine (Azulfidine)
• Intra-abdominal and anal abscess secondary to → Corticosteroids – hydrocortisone (Solu-Cortef)
perforation → Immunomodulators – azathioprine (Imuran),
• Fistulas cyclosporine (Neoral)
• Intestinal obstruction
• Dehydration, fluid and electrolyte imbalances • Surgery
• Malnutrition from malabsorption → Laparoscope-guided strictureplasty – the blocked
or narrowed sections of the intestines are
DIAGNOSTICS widened, leaving the intestines intact.
• Colonoscopy → Bowel resection and anastomosis
• Intestinal biopsies → Colectomy with Ileostomy (colostomy) – surgical
• Stool examination – occult blood removal of a part or all of the colon for severe
• Barium study of the upper GIT showing a classic “string cases
sign” at the terminal ileum indicating a constriction of → Intestinal transplant – for severe cases of
a segment of the intestines. Inflammatory Bowel Disease
• CT-scan and Barium enema to determine ulcerations → Continent Ileostomy (Kock pouch or K pouch) – is
and fistulas a connection of the end of the ileum to the skin of
• CBC – hematocrit and hemoglobin levels, WBC count the abdomen with approximately 30 cm of the
• Serum electrolytes distal ileum is reconstructed to form a reservoir
(pouch) with a valve.
ULCERATIVE COLITIS • This is usually done after a total colectomy. GI
• recurrent (remissions) ulcerative and inflammatory contents can accumulate in the pouch for
disease of the mucosal and submucosal layers of the several hours and then removed by means of
colon and the rectum. It is usually accompanied by catheter inserted into the valve. This
systemic complications. eliminates the need of an external bag.
→ Restorative Proctocolectomy with Ileal Pouch Anal
CLINICAL MANIFESTATIONS Anastomosis
• Left lower quadrant pain • (RPC-IPAA) removes the entire colon and
• Diarrhea, passage of mucus and pus rectum while preserving the anal sphincter
retaining normal bowel function and fecal
• Intermittent tenesmus
continence.
• Rectal bleeding
• The procedure makes an ileal reservoir
• Pallor and anemia
functioning as the new rectum. The pouch
• Anorexia and weight loss
serves as an internal pelvic reservoir for
• Nausea and vomiting intestinal contents.
• Dehydration, Fatigue, Fever

COMPLICATIONS
• Toxic megacolon
• Colonic distention secondary to toxic megacolon
• Perforation and bleeding
• Hypovolemia and shock
• Dehydration, fluid and electrolyte imbalances
 NCM116GEP MIDTERMS

INTESTINAL OBSTRUCTION
• Occurs when blockage prevents the normal flow of
intestinal contents through the intestinal tract.
Etiology:
• Mechanical obstruction – an intraluminal obstruction
from pressure on the intestinal wall occurs. e.g.
polypoid tumors, neoplasm, stenosis, strictures,
adhesions, hernias, abscesses, intussusception
• Functional obstruction – the intestinal musculature
cannot propel the contents along the bowel. e.g.
muscular dystrophy, endocrine disorders like DM,
neurologic disorders like Parkinson’s disease.

SMALL BOWEL OBSTRUCTION

• Most bowel obstructions occur in the small intestine.
• Most common cause: adhesions, hernias and
neoplasms, intussusception, volvulus (twisting of the
bowel) and paralytic ileus.

LARGE BOWEL OBSTRUCTION

• Obstructions in the large intestines commonly occur at
the sigmoid colon.
• The most common causes are: carcinoma,
diverticulitis, inflammatory bowel disorders and benign
tumors.

CLINICAL MANIFESTATIONS
• Crampy and colicky pain
• Absent fecal matter and flatus but may pass blood
• Vomiting
• Fecal vomiting
• Dehydration
• Weight loss, weakness and anorexia
• Abdominal distention

DIAGNOSTICS
• Imaging studies: x-ray, CT-scan, MRI
• Ultrasonography
• CBC and serum electrolytes to monitor for infection and
dehydration

MANAGEMENT
• Bowel decompression and aspiration through NGT
• Fluid and electrolyte replacement
• Surgical management depending on the cause of
obstruction
• Herniorrhaphy
• Adhesiolysis
• Intestinal resection with or without anastomosis
• Monitor for signs of hypovolemic shock
 NCM116GEP MIDTERMS
ACCESSORY ORGAN DISORDERS
PANCREA DISORDERS
EXOCRINE PANCREAS
• secretes enzymes necessary for digestion into the
gastrointestinal tract through the pancreatic duct
Secretions:
• alkaline and electrolyte-rich fluid with high-protein
content
• Amylase – aids in digestion of carbohydrates
• Trypsin – aids in the digestion of proteins
• Lipase – aids in the digestion of fats
DISORDERS OF THE EXOCRINE PANCREAS
PANCREATITIS
• acute or chronic inflammation of the pancreas
• autodigestion of the pancreas
• the pancreatic duct becomes temporarily obstructed,
accompanied by hypersecretion of the exocrine
enzymes of the pancreas
• these enzymes enter the bile duct and together with
the bile reflux into the pancreatic duct
ACUTE PANCREATITIS
• self-digestion of the pancreas by its own enzymes
principally trypsin
• enzymes damage the local blood vessels, and
bleeding and thrombosis can occur
• the tissue may become necrotic, with damage
extending into the retroperitoneal tissues
• Etiology: cholelithiasis, sustained alcohol abuse
• Less common causes: bacterial or viral infection,
duodenitis, blunt abdominal trauma, peptic ulcer
disease, ischemic vascular disease, pancreatic
surgery or instrumentation of the pancreatic duct, use
of corticosteroids, contraceptives and thiazide
diuretics
CLINICAL MANIFESTATIONS
• Severe abdominal pain
• Abdominal distention and decreased peristalsis
• Nausea and vomiting
• Back pain resulting from irritation and edema of the
pancreas
• Ascites and Peritonitis (rigid or board like abdomen)
• Ecchymosis in the flank or around the abdomen
• Hypotension
• Tachycardia, cyanosis and cold clammy skin
• Jaundice caused by obstruction of the bile duct or
pancreatic edema pressing on the duct
COMPLICATIONS
• Pancreatic pseudocysts or abscess
• Acute fluid collection in or near the pancreas
• Multi-Organ failure
• Myocardial and Pulmonary insufficiency, pulmonary
edema
• Hypoxia
• Hyperglycemia
• Shock
• Renal failure
• GI bleeding
DIAGNOSTICS
• Serum amylase and lipase
• Urine amylase
• White blood cell count
• X-rays of the abdomen and chest
• Ultrasound
• CT scan
• Hemoglobin and hematocrit for bleeding monitoring
• ERCP – Endoscopic Retrograde Cholangio-
Pancreatography for identifying gallstone
pancreatitis
MANAGEMENT
• Parenteral nutrition for debilitated patients and with
paralytic ileus
• Pain management with parenteral opioids e.g.
morphine
• Nasogastric suction to relieve nausea and vomiting,
abdominal distention and paralytic ileus.
 NCM116GEP MIDTERMS
• Correction of fluid and blood volume loss and low
albumin levels
• Antibiotic therapy if infection is present
• Insulin therapy for hyperglycemia
• Respiratory care: blood gas monitoring, humidified
oxygen, intubation and mechanical ventilation in
emergency situations
• Biliary drainage
• Bed rest
• IV fluids or blood products for maintaining blood
volume and manage hypovolemia

CHRONIC PANCREATITIS
• an inflammatory disorder characterized by
progressive destruction of the pancreas
• with repeated attacks of pancreatitis, cells are
replaced by fibrous tissue and pressure increases
within the pancreas resulting in obstruction of the
pancreatic and common bile ducts and the
duodenum
• Etiology: excessive and prolonged consumption of
alcohol

CLINICAL MANIFESTATIONS
• Recurring attacks of severe upper abdominal and
back pain
• Nausea and vomiting
• Anorexia and weight loss
• Steatorrhea – high fat content stools

DIAGNOSTICS
• ERCP – Endoscopic Retrograde Cholangio-
Pancreatography the most useful diagnostic study in
chronic pancreatitis
• MRI, CT scan, Ultrasound

MANAGEMENT
• Management of abdominal pain and discomfort
using non- opioid analgesics
• Emphasis on the avoidance of alcohol and foods
causing abdominal pain
• Diet, insulin and OHA’s for DM resulting from
pancreatitis
• Pancreatic enzyme replacement for patients with
malabsorption problems and steatorrhea

Surgical Management:
• Pancreaticojejunostomy (Roux-en-Y) – anastomosis
of the pancreatic duct to the jejunum
• Pancreaticoduodenectomy (Whipple resection) –
removal of the pancreatic head, duodenum and gall
bladder
• Cholecystectomy – is done when chronic
pancreatitis develops as a result of gall bladder
disease
• Sphincterotomy - A cut is done in the sphincter of
Oddi to improve the drainage. A T-tube is usually
placed in the common bile duct, for drainage of bile
postoperatively.
 NCM116GEP MIDTERMS
LIVER DISORDERS
LIVER
• largest gland of the body located behind the ribs in
the upper right portion
• 2 major lobes: Right and Left
• manufactures, stores, alters and excretes a large
number of substances involved in metabolism
Functions:
• Glucose metabolism and regulation of
concentration: through glycogenesis,
glycogenolysis, gluconeogenesis
• Protein metabolism: synthesis of plasma proteins:
albumin, blood clotting factors and etc.
• Ammonia conversion: ammonia, a byproduct of
protein metabolism, is converted into urea which is
then excreted in the urine
• Vitamin and iron storage: vitamin A, B-complex, D
and iron are stored in large amounts in the liver.
• Bile formation: Bile aids in digestion by emulsifying
fats using bile salts.
• Bilirubin excretion: a yellow pigment derived from the
breakdown of hemoglobin. Hepatocytes remove
bilirubin from the blood is carried into the bile for
excretion
• Fat metabolism: fatty acids can be broken down for
the production of energy and ketone bodies when
glucose is limited
• Steroid hormones and drug metabolism: metabolism
of the liver usually results in hormone and drug
inactivation. Drug activation may also occur.
DISORDERS OF THE LIVER
LIVER CIRRHOSIS
• Scarring of the liver
• chronic disease characterized by replacement of
normal liver tissue with diffuse fibrosis (scar tissue)
that disrupts structure and function
• Etiology: Alcohol consumption, exposure to certain
chemicals, infectious schistosomiasis
CLINICAL MANIFESTATIONS
→ LIVER ENLARGEMENT / HEPATOMEGALY
• Liver is large and loaded with fat in the early stages
of cirrhosis. Abdominal pain may be present due to
rapid enlargement of the liver.
→ PORTAL HYPERTENSION
• Increased pressure throughout the portal venous
system that results from obstruction of blood flow
through the damaged liver.
→ INFECTION AND PERITONITIS
• Cause: Bacteremia due to translocation of
intestinal flora (Spontaneous Bacterial Peritonitis).
• Management: Antibiotic therapy is effective in the
treatment and prevention of recurrent episodes.
→ SPLENOMEGALY
• Enlargement of the spleen is caused by portal
hypertension from the shunting of blood into the
splenic vein.
→ ASCITES
• Caused by portal hypertension and resulting
increase in capillary pressure (increased
hydrostatic pressure) and obstruction of venous
blood flow.
Clinical Manifestations:
o increased abdominal girth, rapid weight gain,
shortness of breath, abdominal striae and
distended veins
Diagnostics:
o fluid wave test, shifting dullness upon percussion
Management:
o Dietary modification – sodium restriction
o Use of diuretics
o Bed rest
o Paracentesis
o Transjugular Intrahepatic Portosystemic Shunt
(TIPS) - A cannula is threaded into the portal vein by
the transjugular route. Using an expandable stent,
portal hypertension is reduced with an expandable
stent as intrahepatic shunt.
→ ESOPHAGEAL VARICES
• are portosystemic shunts, abnormal vein
connecting the blood supply returning from the
intestines to the vein returning blood to the heart,
bypassing or shunting the liver.
• Other shunts: caput medusae (umbilical area),
hemorrhoids (anus)
Clinical Manifestations:
o Hematemesis
o melena (black tarry stool)
o shock may be present
Diagnostics:
o Endoscopy – indicated to identify the cause and the
site of bleeding
o Ultrasonography and CT scan
Management:
o IV fluids with electrolytes and volume expanders
o Blood transfusions
o Vasopressin – constricts the distal esophageal and
proximal gastric veins reducing the inflow of blood to
the gastrointestinal circulation and eventually the
portal system reducing the portal pressure
o Octreotide – somatostatin (GHIH) decreases blood
flow to the digestive organs
o Balloon Tamponade - A double balloon tamponade
is used to exert pressure on the upper orifice of the
stomach and against the bleeding varices
o Sclerotherapy - A sclerosing agent is injected
through a fiberoptic endoscope into the bleeding
esophageal varices to promote thrombosis and
eventual sclerosis (hardening of body tissue)
o Esophageal Banding Therapy (Variceal Band
Ligation) - A modified endoscope loaded with an
elastic rubber band is passed through an over tube
directly onto the varices to be banded.
o Transjugular Intrahepatic Portosystemic Shunting -
TIPS procedure can effectively control acute
variceal hemorrhage by rapidly lowering portal
pressure
 NCM116GEP MIDTERMS
→ HEPATIC ENCEPHALOPATHY AND COMA
• Portosystemic Encephalopathy (PSE) is the
neuropsychiatric manifestation of hepatic failure
associated with portal hypertension and the
shunting of blood from the portal venous system into
the systemic circulation to the brain.
• The blood contains toxic byproducts of metabolism
caused by the liver’s inability to detoxify these
Clinical Manifestations:
o impaired memory, shortened attention span, sleep-
wake inversions, brain edema, intracranial
hypertension, seizures, asterixis and coma.
o Fetor Hepaticus - Fecal sweetish odor of the breath
of the patient caused by portosystemic shunting
from portal hypertension. This allows the metabolic
by products of intestinal bacteria to enter into the
lungs.
Diagnostics:
o Electroencephalogram (EEG)
Management:
o Lactulose promote the excretion of ammonia in the
stool reducing serum ammonia levels.
o IV administration of glucose to minimize protein
breakdown
o Administration of vitamins to correct deficiencies
and correction of electrolyte imbalances
o Antibiotic treatment to reduce the levels of
ammonia - forming bacteria in the colon e.g.
neomycin, metronidazole
o Moderate restriction of protein in patients who are
comatose
o Prevention of injury, bleeding and infection
→ JAUNDICE
• abnormally elevated bilirubin concentration in the
blood with body tissues, sclerae and skin become
tinged yellow caused by the inability of the
damaged liver to clear normal amounts of bilirubin
from the blood.
→ EDEMA AND BLEEDING
• Hypoalbuminemia due to decreased hepatic
production of albumin develop generalized edema.
• The production of blood clotting factors using
vitamin K by the liver is also reduced, leading to an
increased incidence of bruising, epistaxis, GI
bleeding and bleeding from wounds.
• Management: Low sodium diet, diuretics, vitamin K
→ VITAMIN DEFICIENCY AND ANEMIA
• Impaired absorption of fat-soluble vitamins (A, D, E
and K) as well as dietary fats is present due to
decreased secretion of bile salts into the intestines.
• Impaired GI function, inadequate dietary intake and
impaired liver function contribute to anemia.
• Management: diet supplemented with vitamins
→ METABOLIC AND ENDOCRINE DISTURBANCES
• Hypoglycemia - decreased hepatic glycogen and
decreased gluconeogenesis.
Hyperglycemia
→ ORGAN DAMAGE prevents liver to metabolize
hormones
• Aldosterone – salt and water retention of the
kidneys and increased urine potassium excretion.
• Sex Hormones – amenorrhea, loss of libido,
sterility, testicular atrophy, impotence,
gynecomastia
DIAGNOSTICS
LIVER FUNCTION TESTS
• Serum Aminotransferase (serum enzyme activity)
sensitive indicators of injury to the liver cells:
1. ALANINE AMINOTRANSFERASE (ALT) / SERUM
GLUTAMIC PYRUVIC TRANSAMINASE (SGPT)
→ ALT levels increase primarily in liver disorders
and may be used to monitor the course of
hepatitis or cirrhosis or effects of treatment toxic
to the liver
2. ASPARTATE AMINOTRANSFERASE (AST) / SERUM
GLUTAMIC OXALOACETIC TRANSAMINASE (SGOT)
→ AST is present in tissues that have high metabolic
activity, the level may be increased if there is
damage or death to organs like the liver, heart,
skeletal muscles and kidney
3. GAMMA-GLUTAMYL TRANSPEPTIDASE (GGT)
→ Increased GGT levels are associated with
intrahepatic (liver disease) or extrahepatic
(obstruction of biliary tree) cholestasis
(reduction or stoppage of bile flow) and alcoholic
liver disease.
• Serum Protein Concentrations - serum albumin,
serum globulin, total serum protein
• Pigment Studies - serum direct bilirubin, serum total
bilirubin, urine bilirubin
→ These studies measure the ability of the liver to
conjugate and excrete bilirubin. Bilirubin tests
are performed to measure bile excretion or
retention.
• Prothrombin Time - may be prolonged in liver
disease.
• Plasma Ammonia - failure of the liver to convert
ammonia to urea results in increased serum ammonia
levels.
• Serum Alkaline Phosphatase (ALP) - is an enzyme
manufactured in bones, liver, kidneys and intestine
and excreted through the biliary tract.
→ Elevated levels of ALP in the blood are most
commonly caused by liver disease or bone
disorders.
• Liver Biopsy - is the removal of a small amount of liver
tissue usually through needle aspiration.
• Ultrasound, CT Scan, MRI, Laparoscopy - used to
identify normal structures and abnormalities of the
liver and biliary tree
 NCM116GEP MIDTERMS
GALLBLADDER DISORDERS
GALLBLADDER
• The gallbladder functions as a storage depot for bile
(30 to 50 mL).
• Between meals, when the sphincter of Oddi is closed,
bile produced by the hepatocytes enter the
gallbladder.
• During storage, a large portion of the water in bile is
absorbed through the walls of the gallbladder, so that
bile in the gall bladder is five to ten times more
concentrated than that originally secreted by the liver.
Bile composition:
o Water
o Electrolytes (sodium, potassium, calcium, chloride
and bicarbonate)
o Fatty acids
o Cholesterol
o Bilirubin
o Bile salts - together with cholesterol assist in
emulsification of fats in the distal ileum.
DISORDERS OF THE GALLBLADDER
CHOLECYSTITIS
• acute inflammation of the gallbladder causing pain,
tenderness and rigidity of the upper right abdomen
that may radiate to the midsternal area or right
shoulder
Etiology:
• Calculous Cholecystitis – a gallbladder stone
obstructs bile
• Acalculous Cholecystitis – acute gallbladder
inflammation in the absence of obstruction by
gallstones outflow
→ Causes: severe trauma, burns, infection of the
gall bladder usually by enteric microorganisms
e.g. Escherichia coli.
→ Other causes: include gallbladder volvulus or
torsion of the gallbladder, bile stasis (lack of
gallbladder contraction) and increased viscosity
of the bile
CHOLELITHIASIS
• calculi or gallstones form in the gallbladder from the
solid constituents of bile. they vary greatly in shape,
size and composition.
• Etiology: precipitation of substances contained in
bile mainly cholesterol and bilirubin
• commonly affected are women usually older than 40
years of age, multiparous, obese and those taking
contraceptives.
Types of Gallstones:
• Pigment Stones – form when unconjugated pigments
in the bile precipitate to form stones. The risk for
developing stones is increased in patients with
cirrhosis and infections of the biliary tract.
• Cholesterol Stones – form from decreased bile acid
synthesis and increased cholesterol synthesis in the
liver. Cholesterol is insoluble in water and depend on
bile acids for solubility.
CLINICAL MANIFESTATIONS
• Biliary colic (gallstone attack) is when a colic (sudden
pain) occurs due to a gallstone temporarily blocking
the cystic duct. Location: upper right quadrant or
epigastric area, upper back, right shoulder or mid
scapular region.
• Fever
• Anorexia
• Indigestion, nausea and vomiting
• Jaundice
• Changes in urine and stool color
DIAGNOSTICS
• Ultrasonography
• Radionuclide Imaging or Cholescintigraphy
→ a radioactive agent is administered intravenously.
It is taken up by the hepatocytes and excreted
rapidly through the biliary tract. The biliary tract is
then scanned and images of the gallbladder and
biliary tract are obtained.
• Endoscopic Retrograde
Cholangiopancreatography (ERCP)
→ The hepatobiliary system is visualized using a
side-viewing flexible fiberoptic endoscope
inserted through the esophagus to the
descending duodenum.
→ Multiple x-rays are used during ERCP to evaluate
the presence and location of ductal stones.
• Percutaneous Transhepatic Cholangiography
→ This sterile procedure involves the injection of dye
using a flexible needle directly into the biliary
tract. X-rays are taken in multiple projections.
→ This involves fasting, local anesthesia and
moderate sedation.
MANAGEMENT
• Antibiotic therapy as needed for infections causing
inflammation of the gall bladder
• Analgesia for pain and biliary colic
• Low-fat liquid diet right after a gallbladder attack
• Ursodeoxycholic acid (UDCA) and chenodeoxycholic
acid (CDCA) – used to dissolve small cholesterol
gallstones. These inhibit the synthesis and secretion
of cholesterol, desaturating the bile.
• Extracorporeal Shockwave Lithotripsy (Lithotripsy or
ESWL)
→ Non-invasive and uses repeated shockwaves
directed at the gallstones in the gallbladder or
common bile duct to fragment the stones.
 NCM116GEP MIDTERMS
→ The waves are transmitted to the body through a
fluid-filled bag or by immersing the patient in a
water bath.
→ Broken fragments can then pass from the
gallbladder or common bile duct removed via
endoscopy or dissolved with oral bile acids.
• Cholecystectomy
→ The gallbladder is removed through an abdominal
incision after the cystic duct and artery are
ligated.
→ A drain may be used if there is a bile leak which will
close spontaneously after a few days. The drain
prevents the accumulation of bile.
• Laparoscopic Cholecystectomy
→ the new standard therapy for symptomatic
gallstones
→ insertion of a laparoscope through a small
incision near the umbilicus, and surgical
instruments are inserted through several stab
wounds in the upper abdomen.
 NCM116GEP MIDTERMS
MUSCULOSKELETAL DISORDERS
MUSCULOSKELETAL INJURIES SPRAIN
(these usually happen in sports) • injury to ligament, cartilages, and joints.
→ Ligaments connect bone to bone, and tendons
STRAIN connect muscle to bone.
• injury to your muscles and tendons. • "natipalo", you fell on the wrong side.
• "pulled a muscle" • more painful because bones are deep-seated and
• after stretching, madula siya dayon but may mabilin you pull your muscle somehow.
na gamay nga pain • difficulty in movement, problems with mobility and
ambulation will be present.
THREE DEGREES OF STRAIN • presence of inflammatory responses.
DEGREE OF
DEFINITION SIGNS AND SYMPTOMS
STRAIN GRADING SYSTEM USED FOR SPRAINS
GRADE DEFINITION MANIFESTATIONS
mild stretching • gradual onset of
FIRST of the muscle palpation-induced
DEGREE with no loss of tenderness sprain results from
STRAIN range of motion • mild muscle spasm FIRST tears in some
DEGREE fibers of the • mild pain
or ligament and mild,
MILD localized
• edema
• acute pain during the GRADE hematoma • local tenderness
precipitating event
involves formation
• followed by
moderate tenderness at the site
SECOND stretching with increased pain
DEGREE and/or partial • increased edema
and passive ROM
STRAIN tearing of the • tenderness
• edema SECOND
muscle or • pain with motion
tendon • significant muscle DEGREE involves partial
spasm or tearing of the • joint instability
• ecchymosis MODERATE ligament • partial loss of
GRADE normal joint
function
• immediate pain
severe muscle described as tearing, THIRD occurs when a • severe pain
THIRD or tendon snapping or burning DEGREE ligament is • increased edema
DEGREE stretching with • muscle spasm or completely torn or
STRAIN rupturing and • abnormal joint
• ecchymosis SEVERE ruptured
motion
tearing of the GRADE
involved tissue • edema
• loss of function

CAUSE
CAUSE • over twisting of the ligaments, cartilages, and joints
• overstretching of the muscle
• overuse, excessive stress WHAT CAN WE DO TO PREVENT OVER TWISTING?
• callisthenics
WHAT CAN WE DO TO PREVENT OVERSTRETCHING? • constant practice or training
• warm up, stretching
• callisthenics (body weight exercises, like push up, DIAGNOSTICS
burpees, high jumps, etc) • X-ray, CT Scan, MRI

DIAGNOSTICS (not usually done, but can be…) CONTUSION

• X-ray - obtained to rule out bone injury, because an
avulsion fracture (in which a bone fragment is pulled
away from the bone by a tendon) may be associated
with a third-degree strain.
• CT Scan
• MRI - identifies tendon injury, which is not visible in
x-ray.
• injury to the soft tissues and leading to echhymosis
or bruising or hematoma
• hematoma develops from bleeding at the site of
impact, leaving a characteristic
• “black and blue” appearance.
• common in whiplash injury, happens in vehicular
accidents
• usually happens to the head or abdomen

CAUSE
• Blunt force (BLOW, KICK, OR FALL)
 NCM116GEP MIDTERMS
WHAT CAN WE DO TO PREVENT BLUNT FORCE?
• use safety devices/equipment
DIAGNOSTICS
• X-ray
• CT Scan – to view soft tissues
• MRI – preferred in viewing soft tissues
MANAGEMENT
The treatment for contusions, strains, and sprains is
guided by the severity of injury and consists of protecting
from further injury, resting and elevating the affected part,
applying cold, and using a compression bandage.
REST
• activity should be restricted for 1-2 weeks if strain.
Minimum of 3-6 weeks if sprained. If contusion, 4-12
weeks because there is a possible neurological
problem.
• restrict activities that require weight-bearing,
especially in the affected area.
• use assistive devices, either cane, walker, or crutches.
IMMOBILIZE
• activity should be restricted for 1-2 weeks if strain.
Minimum of 3-6 weeks if sprained. If contusion, 4-12
weeks because there is a possible neurological
problem.
• restrict activities that require weight-bearing,
especially in the affected area.
• use assistive devices, either cane, walker, or crutches.
COMPRESS
window period:
• ice compress if there is bleeding as evidenced by
hematoma or actual bleeding to promote
vasoconstriction, applied within 12-24 hours. To
control inflammatory responses. IT SHOULD NOT BE
PLACED LONGER THAN 20 MINUTES AT A TIME.
• warm compress applied after 24 hours. To prevent
edema formation and discomfort. This promotes
circulation since it promotes vasodilation.
ELEVATE
• elevate the affected part, 30 to 45 degrees, landmark is
above the level of the heart. The patient is lying supine.
Two pillows.
JOINT DISLOCATIONS
1. DISLOCATION OF A JOINT
→ a condition in which the articular surfaces of the
distal and proximal bones that form the joint are
no longer in anatomic alignment.
2. SUBLUXATION
→ partial dislocation and does not cause as much
deformity as a complete dislocation.
→ In complete dislocation, the bones are literally
“out of joint.”
3. AVASCULAR NECROSIS (AVN)
→ this develops when a dislocation or subluxation is
not reduced immediately. AVN of bone is caused
by ischemia, which leads to necrosis or death of
the bone cells.
SIGNS AND SYMPTOMS OF TRAUMATIC DISLOCATION
• acute pain
• change in or awkward positioning of the joint
• decreased ROM
DIAGNOSIS
• Bilateral assessment will make apparent the
abnormality in the affected joint.
• X-rays confirm the diagnosis and reveal any
associated fracture
MEDICAL MANAGEMENT
1. The affected joint needs to be immobilized at the scene
and during transport to the hospital. The joint is
immobilized by splints, casts, or traction and is
maintained in a stable position.
2. The dislocation is promptly reduced, and displaced
parts are placed back in proper anatomic position to
preserve joint function.
3. Analgesia, muscle relaxants, and possibly anesthesia
are used to facilitate closed reduction.
4. Neurovascular status is assessed at a minimum of
every 15 minutes until stable.
5. After reduction, if the joint is stable, gentle,
progressive, active and passive movement is begun to
preserve ROM and restore strength.
TENDONS, LIGAMENTS, AND MENISCI INJURIES
1. ROTATOR CUFF TEARS - a rip in a tendon that
connects one of the rotator muscles to the humeral
head.
• ROTATOR CUFF - stabilizes the humeral head and is
composed of four muscles and their tendons that
include the supraspinatus, infraspinatus, teres
minor, and subscapularis muscles.
CAUSES: Rotator cuff tears may result from acute or
chronic stresses on the joint and from:
1. intrinsic (e.g., age-related factors)
2. extrinsic (e.g., overuse, fracture, etc.)
HIP SURGERY OR HIP REPLACEMENT
• insertion or application of prosthesis at the
acetabulum.
• helical screw application; plates, acts as a support or
alignment to prevent further damage; pins;
sometimes the doctors will use bolts to secure the
bones.
NURSING PRIORITIES: HIP SURGERY
DO’s
1. Maintain the patient in a supine position. It is easy to
maintain the abduction of the px’s leg. There will be
no risk for flexion, especially hip flexion. We need to
immobilize and maintain the patient.
 NCM116GEP MIDTERMS
2. If the patient cannot help it, you have to position the
patient in a side-lying position at the unaffected side
to prevent the weight of the patient to complicate
fracture.
3. Maintain the leg abduction, or away from midline,
external rotation of the hips. Place trochanter rolls or
bolster or hotdog pillows between the patients legs.
If trochanter rolls are not available, you can use
rolled towels, rolled linens, or sand bags.
4. High seat commode, toilet, or chair.
DONT’s
1. Crossing of the legs leads to adduction. We should
prevent this since we are preparing the patient for
rehabilitation and ambulation and mobilization.
2. Bending on the waist. The muscles will pull on the
affected hip or joints, which will raise the hip
replacement. This will also damage the sutures and it
is painful for the patient.
3. Low toilet seat, low commode, or low chair.
4. Orthopneic position (this qualifies semi-fowler
position). The hips are flexed in this position.
5. Hip angulation, at 90 degrees or more. This will also
lead to hip flexion.
FRACTURE MANAGEMENT
X-RAY
• In the x-ray of the patient you will see the patient with
the musculoskeletal system problem especially with
fracture nga makita mo da sa x-ray iya line of fracture.
• The location of the fracture
• Tibia is the common area of fracture
CT SCAN or MRI are the definitive diagnostics for
fractures.
BONE SCAN is used for patients with cancer.
• Used to check the density of the bones.
• Usually patients with osteoporosis.
• Diagnostic used for bone cancer
• One area is weak or multiple areas that are weak
already. The opacity of the bone will be seen in the
bone scan.
DIAGNOSTIC EVALUATION
X-RAY STUDIES
• Bone x-rays determine bone density, texture, erosion,
and changes in bone relationships.
• X-ray study of the cortex of the bone reveals any
widening, narrowing, or signs of irregularity.
• Joint x-rays reveal fluid, irregularity, spur formation,
narrowing, and changes in the joint structure.
• Multiple x-rays, with multiple views (e.g., anterior,
posterior, lateral), are needed for full assessment of
the structure being examined.
• Serial x-rays may be indicated to determine the status
of the healing process.
COMPUTED TOMOGRAPHY (CT SCAN)
• may be performed with or without the use of oral or
intravenous (IV) contrast agents, showing a more
detailed cross-sectional image of the body.
• it may be used to visualize and assess tumors; injury
to the soft tissue, ligaments, or tendons; and severe
trauma to the chest, abdomen, pelvis, head, or spinal
cord.
• it is also used to identify the location and extent of
fractures in areas that are difficult to evaluate (e.g.,
acetabulum) and not visible on x-ray.
MAGNETIC RESONANCE IMAGING (MRI)
• a noninvasive imaging technique that uses magnetic
fields and radio waves to create high-resolution
pictures of bones and soft tissues.
• used to visualize and assess torn muscles, ligaments,
and cartilage; herniated discs; and a variety of hip or
pelvic conditions.
• no pain during the procedure
• It may take 30 to 90 minutes to complete the test.
• Because an electromagnet is used, patients with any
metal implants (i.e., cochlear implants), clips, or
pacemakers are not candidates for MRI
• To enhance visualization of anatomic structures, an IV
contrast agent may be used.
OPEN MRI
• they use lower-intensity magnetic fields, which
produce lower-quality images
• advantages of open MRI include increased patient
comfort, reduced problems with claustrophobic
reactions, and reduced noise.
ARTHROGRAPHY
• used to identify the cause of any unexplained joint
pain and progression of joint disease.
• a radiopaque contrast agent or air is injected into the
joint cavity to visualize the joint structures, such as
the ligaments, cartilage, tendons, and joint capsule.
• joint is put through its range of motion to distribute the
contrast agent while a series of x-rays are obtained.
• if a tear is present, the contrast agent leaks out of the
joint and is evident on the x-ray image.
BONE DENSITOMETRY
• used to evaluate BMD. This can be performed through
the use of x-rays or ultrasound.
• may vary among different skeletal areas; therefore,
BMD results may be normal at one site but low at
another. Because these tests only measure density at
specific sites, they may miss abnormal findings in
other skeletal areas.
FRACTURE
• break in line continuity
CAUSES
1. Extreme muscle contraction
2. Sudden twisted motion
3. Crashing force
4. Direct blows
5. Diseases
 NCM116GEP MIDTERMS

EXAMPLES: 3. LONGITUDINAL FRACTURE

OSTEOPOROSIS → Following along the axis of the bone
• Osteo – bone → May be middle and bilateral
• Poros/Porosis – bone became porous, brittle or weak
4. SPIRAL FRACTURE
PAGET’S DISEASE (osteitis deformans) → It is happening in the bone
• Pag nag break in the bone. Pag nag regrow since our → In the twisting (may be due to physical abuse)
bone is capable or remodeling, bone construction and → Commonly see in abused women/children
repairing as it is/was → Usually in legs and arms
• But in Paget’s Disease may mga extra bone nga ga → There is displacement or misalignment in the bone
form
→ Either OBLIQUE/TRANSVERSE seen on x-ray but
• May deformities also sometimes indi siya ma form as
with MISALIGNMENT
a whole may mga kulang kulang
5. IMPACTED OR TELESCOPING FRACTURE
OSTEOGENESIS IMPERFECTA
→ There is telescoping of the bones
• Congenital anomaly
→ Bone is inserted because of fracture, velocity,
• Bones of infant are fragile that makes them prone to
force, blow
injury/fractures
→ Complete fracture but impacted more inside
TYPES OF FRACTURES → Total separation
SKIN INVOLVEMENT → Lacerated bone, has uneven edges
1. CLOSED OR SIMPLE FRACTURE
→ Intact skin over the area 6. COMMINUTED FRACTURE
→ No break in skin integrity → Fragmented
→ Presence of small cracks on the bone seen in x-ray → Cut into small pieces
→ Can be found in stress fracture → Seen in injuries, trauma, domestic violence

2. OPEN OR COMPOUND FRACTURE SIGNS AND SYMPTOMS OF FRACTURE

→ There is skin penetration and damage 1) CREPITATION/CREPITUS – clicking sound upon
touching
→ either caused by object from outside that’s
2) SHORTENING OF THE LIMB – because of muscle
penetrating the skin going to the bone
spasm
→ or the other way around, in which because of the
→ Edema because there is inflammation.
blow or trauma, the bone breaks the skin,
Inflammatory processes have started so may
penetrating through it
edema.
→ This limb will appear shorter because of the
DEGREES OF SEPARATION
muscle spasm around the fractured area.
1. COMPLETE FRACTURE
→ Immobilize or ice
→ Total separation of fractured part
→ Application of hot and cold compress vary
2. INCOMPLETE FRACTURE depends on the case of the patient
→ Partial separation of fractured part 3) EXTREME PAIN AND ECCHYMOSIS/HEMATOMA –
There is extreme pain of the fractured area because
→ Present in patient with GREENSTICK FRACTURES
there is damage to the neurovascular cells. The
affected area are highly vascularized and highly
GREENSTICK FRACTURE
innervated. It will send a signal to the brain that
• there is only one side of the bone that is bent or
there is something wrong with the limb of the patient
cracked or fractured, commonly seen in children
or hand.
and related to OSTEOGENESIS IMPERFECTA
→ APPEARANCE OF ECCHYMOSIS/HEMATOMA is an
• MANAGEMENT: Padding
indication that the immune system or immune
response is being activated in the body.
LINE OF BREAKAGE
4) ABNORMAL MOTION – “Impaired physical mobility”
1. TRANSVERSE FRACTURE
5) NO PULSE – if the damage is so severe
→ Straight across the bone
→ Commonly related to accident or trauma
→ Could be: CLOSED/SIMPLE,
COMPLETE/INCOMPLETE, or OPEN/COMPOUND

2. OBLIQUE FRACTURE
→ Slanted or a little angled
→ Commonly seen in injury and accident
→ Diagonal
 NCM116GEP MIDTERMS
6 P'S - INDICATION OF COMPARTMENT SYNDROME
PAIN - 1st thing to appear/patient will complain about
• Pain because there is activation of pain receptors or
pain mediators
PARESTHESIA – numbness/weakness of the affected
area.
• PRESSURE - because of the activation of the
immune response
PULSELESSNESS – compression of blood vessels,
below the area of trauma
• PRESSURE will cause the pulselessness
PALLOR – compression of blood vessels, pressure,
below the area of trauma
• PRESSURE is the root cause of the problem and
CAUSE of the compartment syndrome
PARALYSIS – compression of nerves or direct damage to
the nerves
POIKILOTHERMIA – below area of trauma
• Poikilothermia is related to pallor because of the
compression of the blood vessels and there is NO
BLOOD SUPPLY anymore.
• There is too much pressure in the affected area and
below that.
• Able to feel poikilothermia below the affected area.
• Also, there is presence of coolness (.5 to 10
degrees)
• Lower temperature compared to the rest of the body
especially the core temperature
2) TRACTION
• Skeletal Traction - the affected area of the trauma is
usually being pulled
• Skin Traction - only with the use of bandages or leg
stocking
IMPORTANT THINGS TO REMEMBER IN TRACTION:
→ TO MAINTAIN WEIGHTS HANGING FREELY
→ NEVER REMOVE THE WEIGHTS
→ NEVER ATTEMPT TO LIFT THE WEIGHT
→ NEVER ATTEMPT TO LIFT THE SAND BAGS
NURSING PRIORITY IN TRACTION: Support this area with
a pillow and turn every 2hrs.
3) MANUAL MANIPULATION - most common in ER
• there is manual manipulation done by doctor (pulls
limbs)
• teach patient to breathe deeply and exhale as
doctors puts (pulls) limb/bone back in place
FOR OPEN FRACTURES
OPEN REDUCTION
A. OREF — Open Reduction with External Fixation
• doctor opens affected area to place
pins/screws/plates
• to immobilize and align the bones externally done
with patient with open fractures, transverse
fracture, simple transverse fracture
B. ORIF — Open Reduction with Internal Fixation
• placing bone back into its original position using
screws and metal plate

CAPILLARY REFILL - poor perfusion to distal areas

• a good indication of compartment syndrome or
good indication of the presence of 6 P's/ or damage
to the area.
• patients with compartment syndrome after or
following a fracture 5 to 8 seconds sometimes 10
seconds.

NURSING MANAGEMENT
• Promoting immobilization and support of affected
limb/area
• It is important that if the patient has a fracture we
would like to immobilize that area.

FOR CLOSED FRACTURES (no surgery needed)

1) CASTING - It is the most effective way of
immobilizing.

• Fiber glass cast — it is easily dried & light weight but

it is expensive (4x price the plaster)
• Plaster cast — takes longer time but cheaper and
heavy.
NCM116GEP MIDTERMS