GI disorders Flashcards
Cirrhosis - Later Clinical Manifestations
Cirrhosis - most common causes
- Alcoholism
- Hepatitis B & C
- Hepatotoxic meds
Cirrhosis - patho
Infiltration + accumulation of fatty deposits - fibrotic changes - destroy hepatocytes = widespread scar formation - decreased liver function - obstructed blood flow - increased portal pressure
Cirrhosis - S/s early
Anorexia
Generalized fatigue
Abdominal pain
GI symptoms - N+V, diarrhea
Cirrhosis - S/s - disease progression
Weight loss
Bleeding
Jaundice
Ascites
Esophageal varices
Portal HTN
Telengiectasis (spider angiomas)
Cirrhosis - Jaundice (Icterus) - causes & S/s
Obstructed billary ducts
Liver cannot breakdown old RBCs
- Steatorrhea - white, clay color stool - bile needed to break down fat
- Dark urine (maple syrup) - kidneys filter elevated billirubin from blood
- Pruritus
Cirrhosis - Ascites - patho
increased hydrostatic pressure from portal HTN → blood proteins leak into peritoneum; liver unable to synthesize protein → low blood albumin; fluid shifts out of vascular
system into peritoneum → third-spacing occurs; liver cannot metabolize aldosterone → kidneys
retain Na & water; increased vascular volume → further leakage of fluid into abdominal cavity
Cirrhosis - Ascites - S/s
Weight gain
Abdominal (umbilical) hernias
Abdominal distention
Cirrhosis - Ascites - TX
- Low sodium diet
- Aldosterone antagonist - Spironolactone (Aldactone)
- Paracentesis - symptomatic relief - sitting up or side lying ; suprapubic - empty bladder ; Monitor - VS, weight (pre and post), I+O, electrolytes
- Refractory ascites - TIPS - catheter and shunt within hepatic system - connects to the jugular
Cirrhosis - Portal HTN - patho
increased pressure from fibrotic changes → back-up of blood in GIsystem → splenomegaly; veins in esophagus, stomach, intestines, abdominal wall & rectum
dilate → esophageal varices, prominent abdominal veins, hemorrhoids, ascites.
Cirrhosis - Esophageal varices
Patho - thinner, less elastic esophageal veins unable to compensate for increasedpressure → pressure increases, varices enlarge, begin to bleed
- Frank hematemesis - vomitting blood
- Coffee-ground emesis
- Melena, (black tarry stools)
Cirrhosis - Esophageal varices and portal HTN - TX
- Reduce portal HTN - beta-blockers + nitrates
- EGD + banding or ligation
- EGD + Sclerotherapy
- Acute !!! - vasoconstrictive meds - IV - Vasopressin or octreotide
- Sengstaken-Blakemore or Minnesota tube - Airway !!!- pt intubated, on the vent, sedated
Esophageal varices - IV Vasopressin vs IV Octreotide
- IV Vasopressin - systemic - can worsen portal HTN
- IV Octreotide (Sandostatin) - specific - constricts just GI area
Cirrhosis - Hepatic Encephalopathy - patho
Elevated ammonia & toxins in blood
- Ammonia - by-product of digestion of dietary & blood proteins
- Ammonia absorbed from intestinal tract not metabolized by diseased liver
- Ammonia accumulates in blood
a. Altered mental states: Confusion → coma
b. Asterixis - flapping tremor of hands - High protein diet & GI bleeding - aggravate condition (more protein)
Cirrhosis - Hepatic Encephalopathy - TX
- Lactulose
- Low protein diet ; early in cirrhois - high protein
- Neomycin - antibiotic - decrease bacterial flora needed to breakdown protein
Lactulose
Promote excretion of ammonia ; tx of constipation
Improvement in mental status
Expect 2-3 soft stools/day
Watch for diarrhea
Coma - NG, rectal
Cirrhosis DX
- LABS: Liver function panel, serum ammonia, clotting studies, protein + albumin, bilirubin , CBC, H+H, vitamin deficiencies
- CT, MRI, US
- Liver biopsy - Definitive !!! - supine, arm elevated behind head , US guided, between ribs - BLEEDING - stay for 6 hrs, H+H compared
Liver Functions
- _ Metabolism :_Glucose, fat, proteins
- _Conversion: _Ammonia to urea
- _Detoxification: _Drugs, alcohol, toxins
- _Breakdown of RBCs: _Formation of bile
- Production:** **Clotting factors, blood proteins, enzymes **
Hepatitis A (HAV) - causes
Transmitted by the fecal-oral route
1. Non-life threatening, usually self-limiting
HAV - Prevention
- Good hand washing
- Avoid contaminated food & water
- If exposed, receive IgG within 2 weeks
- Get vaccinated (HAVRIX & VAQTA) if:
a. traveling to areas with high incidence
b. living in crowded conditions
c. working in correctional facilities, day-care centers, long-tem care
Hepatitis B (HBV) - causes
Transmitted through blood & serum
- Unprotected sex
- Sharing needles or through accidental needle sticks
- Blood transfusions before 1992
- Hemodialysis
- Maternal-fetal route
- Cosmetic procedure like tattooing & body piercing
HBV - Prevention
- Avoid exposure to blood & body fluids
- Follow standard precaution
- Use needless systems
- Get Vaccinated - 3 doses - 1st; 2nd 1 mo later; 3rd 2 mo after 2nd.
Hepatitis C (HCV) - causes
Transmitted blood to blood
- Sharing needles - illicit drug users have highest incidence
- Receiving blood products or organ transplant before 1992
- Unsanitary tattoo or piercing equipment
- Sharing tools for snorting cocaine
HCV - Prevention and labs
Education of high-risk groups
- Enzyme-linked immunosorbent assay (ELISA)
- Recombinant immunoblot assay (RIBA)
Liver biopsy
Chronic hepatitis - TX
A. Rest - promote regeneration & healing, reduce metabolic demands on liver
B. Nutrition - high CHO, normal protein & fat content, small freq meals
C. Medications
1. Antiemetics
2. Antiviral drugs - reduce the viral load
Antiretroviral agents
3. Immunomodulator
Chronic hepatitis - Education
- Prevent spread of infection
- Avoid alcohol and OTC mediations (acetaminophen)
- If traveling - drink bottle water, or water from purification system, avoid foods washed or prepared with tap water (fresh fruits & vegetables)
* Complications - cirrhosis & liver cancer
Hepatitis - causes
Viral (most common), hepatotoxic medications, alcohol, altered immune
responses environmental toxins
Hepatitis - patho
- liver becomes enlarged & congested with
inflammatory cells, lymphocytes & fluid; widespread inflammation & edema leads to
increased pressure within liver portal system, interferes with blood flow → ischemia &
necrosis; edema of the biliary ducts → obstruction & jaundice
Primary liver cancer
- two types
- Hepatocellular carcinoma - develops from hepatocytes
a. 90% linked to chronic viral hepatitis, & cirrhosis. - Cholangiocarcinoma - originates from bile duct cells
Liver Biopsy - definitive diagnosis
Treatment - palliative
- Surgery
- Chemotherapy and hepatic artery embolization
- Liver transplant
Pancreatitis - patho
Autodigestion of pancreatic tissue by pancreatic enzymes
a. Obstruction of the pancreatic duct → increased production of pancreatic enzymes (lipase, trypsin, kallikrein). Activation of enzymes → vasodilation,
increased vascular permeability, edema, necrosis & hemorrhage
Pancreatitis - causes
- Cholelithiasis
- Alcohol & drug use
- Pancreatic tumors or cysts
- Abdominal trauma, surgical manipulation
- Infection
- Corticosteroids, Thiazide diuretics (Hydrochlorothiazide)
Pancreatitis - Pain
Severe pain
a. Midepigastric or LUQ pain - can radiate to the back or left shoulder
b. N & V
c. Assume fetal position
Pancreatitis - Pain TX
- NPO – bowel rest; possible NG tube
- IV hydration
- Analgesics – Dilaudid, Morphine, Fentanyl, Dilaudid
- Anticholinergics - Bentyl, Pro-Banthine
- Antisecretory agents - somatostatin & octreotide
- Antiemetic
- PPIs & H2 blockers
- Antispasmodic (Vistaril, Atarax)
Bentyl & Pro-Banthine
Anticholinergic - decrease GI motility - decrease secretion of pancreatic enzymes
TX of pancreatic pain
SE - dry mouth
- Serum amylase
- Serum lipase
- elevated 1st
- more DX - elevated for longer
* Classic labs for pancreatitis
In addition - Hypocalcemia - Tetany (Chvostek’s and Trousseau’s sign).
Pancreatitis - Complications
- Hypovolemia, hemorrhage & shock
- Acute renal failure
- Respiratory complications - pleural effusion, atelectasis, & pneumonia, leading to ARDS
- DIC
- Diabetes mellitus
- Sepsis & Multi-organ system failure (MOSF)
Pancreatitis - Diet
- Small frequent meals - 4-6 times/day
- Low fat, high carbs and protein
- Bland food - no spices or stimulants
Pancreas - function
- Exocrine gland enzymes - help break down carbohydrates, fats, proteins, and acids in the duodenum. These enzymes travel down the pancreatic duct into the bile duct in an inactive form. When they enter the duodenum, they are activated. The exocrine tissue also secretes a bicarbonate to neutralize stomach acid in the duodenum.
- Endocrine gland hormones - insulin and glucagon (which regulate the level of glucose in the blood), and somatostatin (which prevents the release of the other two hormones).
- Turner’s sign
- Cullen’s sign
- flank discoloration (ecchymosis)
- periumbilical ecchymosis
** Necrotizing, hemorrhagic pancreatitis
Cholecystitis vs Cholelithiasis
inflammation of the GB vs stones in the gallbladder
Bile function
is the greenish-yellow fluid (consisting of waste products, cholesterol, and bile salts) that is secreted by the liver cells to perform two primary functions, including the following:
To carry away waste
To break down fats during digestion
Biliary system function
bile ducts, gallbladder, and associated structures
To drain waste products from the liver into the duodenum
To help in digestion with the controlled release of bile
Stone formation & pathophysiology
a. abnormal metabolism of cholesterol & bile salts
b. Stones form → irritate the GB wall → inflammation. Stones block cystic duct → trapped bile causes chemical irritation of GB. Irritation → edema &
distention → interferes with circulation. Infection & ischemia → necrosis &
gangrene. Severe edema → perforation & peritonitis
GB disease - S/s
1.GI distress - dyspepsia; bloating & flatulence; N & V
2. Pain - Biliary colic
3. Fever - Tachycardia
4.Jaundice - pruritus; dark urine; steatorrhea;
impaired absorption of fat soluble vitamins
GB disease - Somatostatin + Octreotide
antisecretory agents, antiinflammatory properties - used to decrease risk of pancreatitis with Endoscopic retrograde cholangiopancreatography (ERCP)
Crohn’s - common location + appearance
Ileocecal area (RLQ)
Patchy, cobblestone appearence, edematous
Crohn’s - S/s
- Diarrhea - 5-6 loose stools - non bloody
- Weight loss
- Nutritional deficiencies - anemia, low albumin; steatorrhea
- Pain - RLQ
- Fever + leukocytosis
Crohn’s - complications
Fistulas & abcesses - peritonitis/perforation
Crohn’s - DX
CBC, ESR + CRP. electrolytes, Imaging studies, albumin, folic acid, B12, iron
Endoscopy
Crohn’s & Ulcerative colitis - TX
- Aminosalicylates - 5 ASA
- Steroids
- Immunomodulators
- Antidiarrheals
- Anti-infective - tx fistulas + abcesses
Sulfasalazine (Azulfidine)
Aminosalicylates - 5 ASA - inhibit prostaglandins - anti-inflammatory effect
tx of Crohn’s + Ulcerative Colitis
Assess for sulfa allergies
PO - full glass of water - to avoid crystallization of the urine
Takes 2-4 weeks to work
Balsalazide vs Mesalamine (Ascol)
works in colon - tx of ulcerative colitis
vs
works in terminal ileum - tx of Crohn’s
* Fluids to avoid crystallization of the urine
Aminosalicylates - 4 ASA
Infliximab (Remicade) - IV
and
Humira - subcut
Immunomodulators - tx of Crohn’s + Ulcerative Colitis
Lomotil
and
Imodium
Antidiarrheals - tx Crohn’s
Caution - Ulcerative colitis - Toxic megacolon !!! - dilation of the colon - perforation
Ulcerative Colitis - common location + appearance
Rectosigmoid colon (end of large intestine) - LLQ
Very red, edematous, continuous
Ulcerative Colitis - S/s
- Up to 20 diarrhea stools/day - bloody + mucus stools
- Weight loss
- Pain LLQ
- Tenesmus - urgent sensation to defecate
- Extraintestinal symptoms
Arthritis
Oral lesions
Cholelithiasis
Ulcerative Colitis - complications
Hemorrhage
Abcesses
Sclerosing cholangitis - inflammation of the gallblader and ducts around it
Increased risk for colon cancer
Ulcerative Colitis - DX
….
+ Liver panel and Colonoscopy /Bx
Diverticula - common location and cause
Herniations or out-pouching of the intestinal wall
sigmoid colon
Low fiber diet
Evident in 50 % of people over 80
DX: colonoscopy
Diverticulosis vs Diverticulitis
Presence of many herniations
vs
Inflammation of one or more deverticula
Diverticula - TX
- Bowel rest - NPO - progress to clear liquids, low fiber diet - teach about increasing fiber gradually - 25-30 grams
- Anti-infectives - Flagyl or Cipro
Colon Cancer - Risk
Family hx of polyps
Hx of ulcerative colitis
Age over 50, male
Diet - high fat, red meat, processed carbs, low fiber, fried + grilled foods.
Smoking
Familial adenomatous polyposis FAP
Colon Cancer - 55 % in rectosigmoid colon - S/s
- Rectal bleeding - Hematochezia - bright red blood
- Stool narrow, ribbon-like
- Straining to defecate
Colon Cancer - ascending colon - S/s
- Rectal bleeding - black, tarry, mahogany color
- Anemia
- Little change in stool appearance
Colon Cancer - DX
A. Labs - CBC, FOBT, CEA ( carcino-embrionic antigen)
B. Imaging Studies - Barium enema, CT, MRI
C. Procedures - Colonoscopy & sigmoidoscopy - direct visualization of the colon
FOBT - fecal occult blood test
Hemoccult test
Don’t eat red meat or anything red
Do not contaminate with tissue or urine
No NSAIDs or Steroids - GI irritation
No Vitamins
* Do not stop medication - keep in mind
Colonoscopy - pre-care & during procedure
-
Pre-care*
1) Informed consent
2) NPO for 8 hours, except for certain medications
3) Cleanse bowel
a. Oral Go-Lytely
b. Enemas until clear
4) Establish IV access
-
During procedure*
1) Administer oxygen & sedation - Benzodiazepines - Versed, Valium, Fentanyl
2) Monitor airway & VS
Colonoscopy - post-care
Monitor VS frequently, q 15-30 minutes
a. Assess sedation levels and assess for any complications
b. Assess for rectal bleeding
c. Assist out-of-bed (OOB) to assess stability
Pain - expected - intermittent gassy, crampy pain
!!! Continuous pain - rigid abdomen - perforated colon ?
The American Joint Committee on Cancer TNM staging system
- T (tumor) - how far the primary tumor has grown into the wall of the intestine;
has it spread locally to nearby areas. - N (nodes) - extent of spread to nearby lymph nodes
- M (metastasis) - indicates if cancer has metastasized to other organs
Hemicolectomy with anastomosis - laparascopic - post-care
remove tumor - reconect healthy pieces together + remove lymph nodes
- Incision
- Bowel sounds - absent or hypoactive for 24-48 hrs - NPO until return (ice chips)
- NG - decompress the bowel - prevent N+V
- Colostomy - maybe
- Pain - epidural PCA - assess pain + insertion site ; should be able to ambulate - moniot RR + Vitals + level of sedation
- Antibiotics - 24 hrs
Teaching on screening guidelines for colorectal cancer
Colonoscopy every year
Start screening age 50 unless high risk - Repeat every 10 years
Stop at age 75
Flexible Sigmoidoscopy can be done instead (at the doctor’s office)
TPN - best practices
A. Check physician’s order and compare order with TPN formula
1) A new order must be written every day
B. Keep the solution refrigerated until ready to use
C. Wash hands, use aseptic technique, attach proper tubing with the appropriate filter to
solution bag
D. Regulate flow on an IV infusion pump
E. Monitor for complications and response to therapy
F. Assess daily labs, monitor daily weights and I & O
1) Blood sugars q 6 h with insulin coverage
G. Replace TPN/Lipid solutions and tubing q24h
1) Label bag with start & stop times
H. If next bag is not available, discontinue current bag, hang 10% or 20% dextrose
I. Never increase IV rate to “catch-up”
TPN - complications
1) Solution related - fluid & electrolyte imbalances
a. Hyperosmolar solution can cause fluid shifts resulting in hyper or hypovolemia
b. Hyperglycemia can cause osmotic diuresis leading to dehydration & hypovolemia
c. Sodium, potassium & calcium imbalances can occur
2) Infections
a. Contaminated solutions and IV catheters
i. strict aseptic technique is required when handling and
administering TPN.
GI - Age related changes
A. Poor dentition or ill-fitting dentures
B. Diminished sense of taste
C. Atrophy of the gastric mucosa
Decreased production of hydrochloric acid
a. less absorption of iron and cobalamin (vitamin B12)
D. Reduced GI motility
E. Loss of sphincter tone
F. Change in the structure/function of the pancreatic duct
G. Decrease in liver cells
Liver enzymes
- Aspartate aminotransferase (AST)
- Alanine aminotransferase (ALT)
- Alkaline phosphatase (ALP)
- Lactic dehydrogenase (LDH)
Esophagogastroduodenoscopy (EGD) - visualization of the esophagus, stomach &
duodenum
- *Pre-care**
a. Informed consent
b. NPO for 8 hours, except for certain medications
c. Establish IV access - *_ During procedure_**
a. Administer oxygen & sedation
b. Monitor airway & VS
Post-care
a. Monitor VS frequently, q 15-30 minutes
Assess sedation levels and assess for any complications
b. Keep NPO until the gag reflex returns
Prevent aspiration of food or fluids
c. Assist out-of-bed (OOB) to assess stability
Endoscopic retrograde cholangiopancreatography (ERCP)
EGD with visualization of the biliary and pancreatic ducts using radio opaque dye
Pre & post care - similar to EGD
Additional complications specific to an ERCP
a. gallbladder inflammation & pancreatitis
Liver bipsy - pre-care + post-care
- *Pre-care**
1) Informed consent needed
2) NPO 8 hours
3) Obtain coagulation studies, type & cross match, and baseline CBC
4) Instruct pt on the procedure - *Post-care**
1) Assess VS frequently: q 15 min. x 2, then q 30 min. x4, then q 1 hour x 4.
2) Position
a. right side for 2 hours to splint puncture site, then flat for up to 12 hours
3) Assess puncture site
Hernias
weakness in a muscle wall that allows the partial or complete protrusion of an organ through the weakened area
Signs & symptoms
A. Lump or protrusion
B. Strangulated hernia
1. Abdominal distention, N & V, pain, fever, and tachycardia - tx : resection of the ischemic bowel with temporary colonoscopy
Urinary complications - void within 6-8 hrs
Complications of
intestinal obstructions
acid-base and electrolyte imbalances
Fluid, gas & intestinal contents accumulate proximal to obstruction - Intestinal content not absorbed since fluid cannot move along the GI tract - Distention occurs - Peristalsis increases - release of more secretions, further distention - Edema of bowel, increasing capillary permeability
- Plasma leaks into the peritoneum - loss of fluids & electrolytes
a. Loss of fluid - hypovolemia
b. Loss of electrolytes - acid-base imbalances
Causes - malabsorption syndrome
- Bile salt or enzyme deficiency
a. malabsorption of fats & fat-soluble vitamins
b. lactase deficiency - Bacteria
- Disruption of mucosal lining of intestine
a. Celiac disease, Tropical Sprue, Crohn’s disease & Ulcerative colitis - Decreased lymphatic or vascular flow
- Decrease in stomach or intestinal surface area
a. Gastric or intestinal resection - short bowel syndrome
Lactase deficiency TX
&
Celiac disease TX
Lactose-free or restricted diet
&
Gluten-free diet - Gluten is a protein complex found in wheat (including kamut and spelt), barley, rye and triticale
Oral cancer - risk factors
1) Smoking & chewing tobacco
2) Excessive alcohol use
3) Tanning
4) Strong link with the HPV
GERD - chronic disorder - contributing factors
1) Fatty foods, carbonated beverages
2) Chocolate, peppermint, citrus fruits
3) Smoking, alcohol, obesity
4) Medications
GERD - S/s
A) Dyspepsia - indigestion or heartburn
B) Regurgitation
C) Excessive gas production resulting in burping, bloating & flatus
D) Resp. symptoms may include cough; increased incidence in pts with asthma
GERD - Nonsurgical & nonpharmacological interventions
Dietary & lifestyle modifications
Avoid acidic, irritating foods
Eat 4-6 small meals a day; remain upright for 1-2 hours after meals
Avoid eating anything for 3 hours before bedtime
GERD - Drug therapy & SX
- *Drug therapy**
1. Antacids - neutralize acid in the stomach
2. Histamine (H2) blockers - block the H2 receptors on parietal cells
3. Proton Pump Inhibitors (PPI) - inhibiting the hydrogen/potassium ATPase system
4. Prokinetics (Reglan) - facilitate gastric emptying; increase stomach motility
Surgical
• Laparoscopic Nissen fundoplication - minimally invasive sx - portion of the stomach fundus is wrapped around the lower esophageal sphincter
GERD - complications
1) Esophageal scar tissue - leading to strictures
2) Barrett’s esophagus - pre-malignant condition - the lining of the esophagus is damaged by stomach acid and changed to a lining similar to that of the stomach
Hiatal or diaphragmatic hernias - TX similar to GERD
A) Sliding hernia - esophagogastric junction and the upper stomach, or fundus, freely
move in & out of the chest through the weakened diaphragm
Concern - development of GERD and its complications
B) Rolling hernia - esophagogastric junction remains in place, but the fundus of the
stomach and occasionally the greater curvature of the stomach move through the
diaphragm into the chest
Concerns - volvulus (twisting), obstruction and strangulation
Esophageal cancer - risk factors
1) Smoking & tobacco use
2) Excessive alcohol intake
3) Long-term, untreated GERD
4) Barrett’s esophagus
5) Achalasia (spasm of LES)
6) Esophageal diverticuli
7) HPV
Esophageal cancer - S/s
A) Persistent and progressive dysphagia
1) Difficulty swallowing solids, then progressing to increased difficulty swallowing soft foods, then liquids
B) Weight loss
C) Food sticking in throat
D) Increased pain with swallowing
1) Chest pain, regurgitation
E) Cough & increased secretions
Gastritis - patho
&
Chronic gastritis
Protective barrier is lost, a process called autodigestion → inflammation,
edema, bleeding
Chronic gastritis → progressive atrophy of the mucosal lining, interferes with parietal cell function, → decreases production of HCL and intrinsic factor→ Intrinsic factor is
necessary for the absorption of vitamin B12 → Decreased production of intrinsic factor → cobalamin deficiency and pernicious anemia
Acute gastritis causative factors
1) Stress
2) H.pylori bacteria - gram-negative bacteria that penetrates the mucosal lining
3) Long-term NSAID use
4) Excessive alcohol & caffeine consumption
5) Certain medications such as corticosteroid
a. NSAIDS inhibit prostaglandin production destroying the stomachs protective barrier
Gastric ulcer
vs
Duodenal ulcer
vs
Stress ulcer
delayed stomach emptying
vs
rapid stomach emptying
vs
hospitalized patients
a. NPO status
b. ischemia to mucosal lining
Peptic Ulcer Disease (PUD)
lesion on the gastric or duodenal mucosa
Prilosec - Omeprazole
Nexium - Esomeprazole
- prazole meds
Proton Pump inhibitors
main tx for more severe GERD
long-acting inhibition of gastric acid and secretion by affecting the proton pump of the gastric parietal cells
SE- Hypocalcemia - hip fx
GI infections
Pneumonia
Assessment for perforated diverticulum
Diverticula - food or bacteria trapped - diverticulitis - perforate - local abscess.
A perforated diverticulum can progress to an intra-abdominal perforation with peritonitis
Generalized pain
N&V
Fever low grade - chills + tachycardia
Exam abdomen for profound guarding , rebound tenderness,
! Sepsis, hypotension, hypovolemic shock
Itching with gall bladder issues
Obstructive jaundice - normal flow of bile into duodenum is blocked - allowing excessive bile salts to accumulate in the skin - pruritus or burning sensation
Cholecystitis: inflammation of the GB
Cholelithiasis – stones in the gallbladder
Patho
abnormal metabolism of cholesterol & bile salts
Stones form → irritate the GB wall → inflammation. Stones block cystic duct → trapped bile causes chemical irritation of GB. Irritation → edema & distention → interferes with circulation. Infection & ischemia → necrosis &
gangrene. Severe edema → perforation & peritonitis
Cholecystitis - TX
A. Nonsurgical
a. Analgesics – Dilaudid, Morphine
b. Anticholinergics - Bentyl
c. Low fat diet
B. Surgical
a. Laparoscopic Cholecystectomy
i. Carbon dioxide is instilled
ii. Postop shoulder or scapular pain from CO2
b. Choledochoscopy
i. Exploration of common bile duct – remove stones
c. Extracorporeal shockwave lithotripsy (ESWL)
d. Open cholecystectomy
i. Greater risk for complications
ii. Drains
1. Jackson-Pratt (JP)
2. T-Tube
