GI 3 lecture Flashcards
Intestinal obstruction:
1) Define it
2) Differentiate between the 2 types of small bowel obstruction (SBO)
1) Interruption in normal flow of intraluminal contents
2) Mechanical: intra- or extra-luminal mechanical compression
Functional: dysfunctional peristalsis (ex/ ileus)
True or false: Colorectal obstruction is a type of intestinal obstruction
True
What are the 2 classifications of SBO?
Mechanical
Functional
Mechanical SBO:
1) What causes it?
2) What does it result in?
3) What increases distention?
4) What happens to fluid?
1) Caused by either intrinsic luminal obstruction or extrinsic compression of small bowel
2) Results in progressive dilation proximal to obstruction & decompression distal to obstruction
3) Accumulation of swallowed air & gas from bacterial fermentation increases distention
4) Bowel wall edema, loss of normal absorption, fluid sequestered in lumen, transudative fluid loss into peritoneal cavity
Mechanical SBO:
1) What is the most common cause of ischemic necrosis
2) Excessive dilation can lead to what 2 things?
3) Describe the sequalae
1) Twisting of the bowel and/or its mesentery around an adhesive band or intestinal attachments
2) Compromised intramural vessels & reduced perfusion to bowel wall
3) Decreased perfusion → ischemia → necrosis & perforation
Mechanical SBO: Describe what happens with proximal obstruction
Ongoing emesis → fluid loss (Na, K, H, Cl) → hypovolemia
Possible feculent emesis
Mechanical SBO:
1) What are the most common causes?
2) What are some other causes?
1) Intraperitoneal adhesions (followed by tumors & complicated hernias)
2) Crohn’s disease, volvulus, intussusception, gallstones
List some extrinsic and intrinsic causes of mechanical SBO
1) Extrinsic: adhesions, hernia, volvulus
2) Intrinsic: tumor, stricture, intussusception, gallstones, foreign body
How do most pts with mechanical SBO present?
Acutely with abdominal pain, nausea, vomiting, abdominal distention, obstipation (inability to pass any flatus or stool)
What Hx should you take with mechanical SBO?
History: identify any risk factors
1) Prior abdominal or pelvic surgery (risk for adhesion formation)
2) Abdominal wall or groin hernia
3) Intestinal inflammation (ie, Crohn’s)
4) History of or increased risk for neoplasm
5) Prior abdominopelvic irradiation
6) History of foreign body ingestion
List some systemic signs of acute mechanical SBO you may see on PE
-Dehydration
-Tachycardia
-Orthostatic hypotension
-Reduced urine output
-Dry mucous membranes (severe cases)
-Fever possible with infection
List some other signs you may see for an acute mechanical SBO on PE
1) Abdominal distention
2) Identify surgical scars
3) Auscultation
-High-pitched “tinkling” sounds associated with the pain
-Muffled bowel sounds with significant distention
What are some signs of acute mechanical SBO when you’re palpating?
1) Very TTP diffusely
2) Abdominal wall or groin hernias
3) Abnormal masses
4) Percussion
5) Hyperresonance or tympany
6) Fluid-filled loops will result in dullness
7) Tympany over liver (instead of dullness) may indicate free intraabdominal air
8) Tenderness to light percussion suggests peritonitis
What are some signs of acute mechanical SBO on digital rectal exam (DRE)
1) Fecal impaction
2) Rectal mass
3) Gross or occult blood (tumor, ischemia, inflammatory mucosal injury, intussusception)
What will labs look like with an acute mechanical SBO?
1) CBC with diff: may have leukocytosis with left shift,
2) Electrolytes, BUN, creatinine: severe hypovolemia, hyponatremia, hypokalemia
What will labs look like with an acute mechanical SBO & signs of systemic illness?
1) ABG: metabolic alkalosis from severe vomiting; metabolic acidosis
2) Serum lactate: ischemia
3) Blood cultures: bacteremia
Describe how to perform a CT abdomen with contrast if a pt has an acute mechanical SBO & what you should look for
To further characterize nature, severity, & potential etiologies of obstruction:
1) Perform with PO/IV contrast (if not contraindicated)
2) Omit oral contrast if complete bowel obstruction
3) **Identify specific site (transition point)
4) Severity of obstruction (partial vs complete)
5) Determine etiology: masses, hernias, inflammatory changes
6) Identify complications: ischemia, necrosis, perforation
Describe the initial management of an SBO
1) Admission & surgical consultation
2) Fluid therapy
3) Diet: NPO
4) Gastrointestinal decompression: NG tube
Indications for surgical therapy with an SBO include what?
1) Immediate surgery for suspected bowel compromise (perforation, necrosis, ischemia)
2) Treating surgical correctable cause of SBO
3) Failure of nonoperative management (3-5 days)
Celiac disease:
1) What is it?
2) Give some examples of dietary gluten
1) Small bowel disorder characterized by mucosal inflammation, villous atrophy, & crypt hyperplasia, which occur upon exposure to dietary gluten & demonstrate improvement after withdrawal of gluten from the diet
2) Wheat, barley, & rye
Describe the epidemiology of Celiac disease
1) Primarily in Caucasians of Northern European ancestry
2) Rare in Asians & Africans
3) Increased prevalence with age
40 Prevalence increased with autoimmune diseases
Describe the range of Sx with Celiac disease
Some have classic symptoms of malabsorption; some have mild symptoms
Describe the pathophys of Celiac disease
1) Genetic factors & altered immune function
2) Prevalence up to 10% in 1st degree relatives
3) 90-95% affected carry HLA-DQ2
>90% of remaining 5-10% carry HLA-DQ8
HLA-DQ2 and/or HLA-DQ8 found in >99% Celiac patients
4) Gluten proteins in wheat, barley & rye resist intraluminal digestive processes
Give the classic disease signs of Celiac
Pain-malabsorption with GI symptoms:
Diarrhea, weight loss, excessive flatus, abdominal pain
May have dermatitis herpetiformis
Give the clinical features of non-classic Celiac
Subclinical (asymptomatic)
May have iron, folate or calcium deficiency, osteopenia
What will you see on PE with Celiac disease
Most with silent disease lack exam findings
Weight loss
Muscle wasting
Pallor
Stomatitis
Easy bruising
Dermatitis herpetiformis
Describe serologic evaluation for Celiac disease (on gluten diet!)
Tissue transglutaminase (tTG)-IgA: single preferred test
Total immunoglobulin A (IgA)
If total IgA deficiency, get deamidated gliadin peptide (DGP)-IgG or Endomysial Ab (EMA)-IgA
Describe how to Dx Celiac
Perform serologic testing and EGD with small bowel biopsies for diagnosis
Discordant serology & histology:
If diagnosis still uncertain, send for HLA DQ2/DQ8 testing
Celiac disease is excluded with negative HLA DQ2/DQ8
Describe histology of Celiac
atrophic mucosa, blunted or complete loss of villi
Describe a gluten free diet
Eliminate foods containing wheat, barley, rye, sauces, gravy, and thickened foods. Beware of makeup, toothpaste, salad dressings
Describe how to manage Celiac disease
1) Gluten free diet
2) Treat micronutrient deficiencies: iron & folate deficiency
3) Osteopenia: obtain bone density, supplemental calcium & vitamin D
4) Hypo splenism: (loss of lymphocytes through inflamed bowel mucosa) need a pneumococcal vaccine
Describe the pathogenesis of acute pancreatitis
1) Exact pathogenesis unknown/unclear
2) Possible mechanisms:
Common bile duct edema or obstruction (gallstones)
Bile reflux into pancreatic ducts
Alcohol damages acinar cells that synthesize digestive & lysosomal enzymes which can lead to pancreatitis
List the etiologies of acute pancreatitis
Gallstones (40-70%)
Alcohol (25-35%)
Hypertriglyceridemia (up to 14%)
Post-ERCP (5%)
Genetic risk
Medications (<5%) (GLP-1s, some other diabetic meds)
Idiopathic (15-25% after inconclusive work-up)
Acute pancreatitis:
1) What are some risk factors?
2) Who’s more likely to have a serious course?
3) Describe risk reduction
1) Alcohol, smoking, high dietary glycemic load, abdominal adiposity, hypertriglyceridemia
2) Older age, obesity
3) Vegetable, dietary fiber, statins
What may you see on acute pancreatitis Hx?
Heavy smoker, Heavy alcohol intake
Large meal
Uncontrolled triglycerides
What are some signs and Sx of acute pancreatitis?
Sudden onset severe, steady, boring epigastric pain
Pain often radiates to back
Nausea/vomiting
weakness, sweating, anxiety
What may you see on an acute pancreatitis exam?
1) Tender abdomen, possible distention, possible absent bowel sounds (ileus)
2) Severe cases: fever, tachycardia, hypotension (possible shock), pallor, cool & clammy skin
3) Jaundice (with obstructed CBD)
4) Cullen’s sign or Grey Turner sign in severe necrotizing pancreatitis
List the labs for acute pancreatitis
1) Sr lipase (& amylase) >3x ULN (upper limit normal)
2) Lipase elevated longer and more accurate for diagnosis
3) Possible leukocytosis, proteinuria, hyperglycemia; elevated bilirubin, BUN & ALP
4) If due to hypertriglyceridemia: fasting TG > 1000
Describe how you can assess the severity of acute pancreatitis
1) Several scoring systems to assess severity & injury to other organs
2) None of the systems have a high prognostic accuracy
3) Ranson Criteria (60-80% sensitivity for predicting severe course)
4) BUN elevation to predict mortality
5) CRP elevation
Describe management for mild acute pancreatitis
1) NPO, bedrest, nasogastric suction (severe pain & distension)
2) Morphine for pain
3) Clear liquid diet when pain free & bowel sounds present
4) Advance to low-fat diet, then advance slowly as tolerated
5) 20% have recurrent pain upon refeeding
6) Cholecystectomy before discharge for gallstone-induced pancreatitis
What are some differential diagnoses for acute pancreatitis?
1) Duodenal ulcer
2) Acute cholecystitis
3) Acute intestinal obstruction
Describe imaging for acute pancreatitis
1) IV Contrasted CT abdomen
-U/S not used due to obscuring bowel gas (used to find gallstones)
Describe Tx for severe acute pancreatitis (necrotizing pancreatitis)
1) Aggressive fluid resuscitation
2) ICU
3) Vasopressors may be required
4) Enteral nutrition (NG, NJ) if without oral nutrition 7-10 days
5) May require parenteral nutrition (lipids)
What are some complications of acute pancreatitis?
1) Intravascular volume loss & ileus may cause pre-renal azotemia & acute tubular necrosis (ATN)
2) Fluid collections, necrosis, infection
3) Acute respiratory distress syndrome (ARDS)
4) Pancreatic abscess
5) Pseudocysts
6) Chronic pancreatitis 10%
Describe the prognosis for acute pancreatitis
1) 5% mortality
2) 20% for severe disease (>3 Ranson’s criteria)
3) 25% recurrence with alcohol (40% if also smoking)
4) Chronic pancreatitis
-36% of all patients with recurrent acute pancreatitis
-Alcohol & smoking main risk factors
Chronic pancreatitis: What is it?
A progressive inflammatory disorder resulting from ongoing/recurrent inflammation and loss of functional pancreatic tissue
What are some etiologies of chronic pancreatitis?
1) Chronic alcohol use
2) Smoking
3) Hyperparathyroidism
4) Stricture, stone or tumor (obstructing pancreatitis)
5) Autoimmune pancreatitis
List the S/Sx of chronic pancreatitis
1) Persistent or recurrent episodes epigastric/LUQ pain through to back
2) Anorexia, nausea, vomiting, constipation, flatulence, & weight loss development of insulin-dependent diabetes
3) Steatorrhea may occur late in the course (pancreatic insufficiency)
4) Pain, severe, duration a few hours to months
5) Pain may be continuous
What will you see on exam with chronic pancreatitis?
tenderness over the pancreas, guarding, & ileus
List the labs for chronic pancreatitis
1) Sr amylase & lipase
2) LFTs & bilirubin elevation due to bile duct compression/obstruction
3) Possible excess fecal fat
Describe the imaging for chronic pancreatitis
1) Plain films: calcifications in 30% (pancreaticolithiasis)
2) CT: calcifications, ductal dilatation, heterogeneity or atrophy, cysts, pseudocysts; findings may raise suspicion for cancer
3) ERCP: most sensitive study; infrequently used only for diagnosis
4) MRCP & EUS: less invasive alternatives to ERCP
Chronic pancreatitis: Describe Exocrine pancreatic insufficiency (EPI)
1) Protein malabsorption & fat deficiency
2) Occurs after more than 90% pancreatic function is lost
3) Steatorrhea: poorly-formed, greasy, malodorous stools; float, stick to sides of bowl, difficult to flush
Why is pain management difficult for chronic pancreatitis?
1) Variable response to analgesia
2) Multiple factors contributing to pain
3) Many patients are heavy alcohol users
Describe how to manage chronic pancreatitis
1) Low-fat diet
2) Absolute cessation from alcohol!
3) Opioids should be avoided
4) Tylenol, NSAIDs, tramadol, TCA, SSRI, gabapentin, pregabalin
5) Exocrine pancreatic insufficiency: chronic diarrhea-need to rx pancreatic enzymes
6) Treat associated diabetes
7) Idiopathic: pain may respond to enzyme replacement
Describe Endoscopic therapy (50% success rate) for chronic pancreatitis
1) Treat biliary tract disease
2) Drain pseudocysts (symptomatic, > 6 cm)
3) Eliminate obstruction of pancreatic duct
-Stent placement
-dilation
Most common abdominal surgical emergency is what?
Acute appendicitis
Describe the epidemiology of acute appendicitis
1) Most common abdominal surgical emergency
2) 10% of population
3) Most commonly occurs 10-30 y/o
4) Highest incidence in 10-19 y/o
5) Male>female ratio 1.4:1
6) Lifetime incidence: men 8.6%, women 6.7%
Describe the pathogenesis of acute appendicitis
1) Luminal obstruction: fecalith, calculi, mural inflammation, lymphoid hyperplasia, infectious processes, benign or malignant tumors foreign body
2) Inflammatory process: Inflammation of appendiceal wall → localized ischemia → perforation → abscess or generalized peritonitis
What are the clinical features of acute appendicitis?
1) HPI & pain can vary based on location of appendix
2) RLQ pain (begins periumbilical then localizes to McBurney’s point)
3) Anorexia
4) Nausea and vomiting
5) Possible indigestion, bowel irregularity, diarrhea, generalized malaise
6) +/- low-grade fever
How do you eval for acute appendicitis?
1) McBurney’s point tenderness, + Rovsing’s sign, Psoas sign, and Obturator signs
2) + leukocytosis with left shift
3) Mostly normal UA & chemistries
4) Pregnancy test on all women of child-bearing age
5) U/S or CT
6) Multiple differential diagnoses
7) Unique presentations based on location of appendix
Describe Rosving’s sign for acute appendicitis
1) Indirect tenderness
2) Pain in RLQ with palpation of LLQ
3) Indicates right-sided local peritoneal irritation
Describe the PSOAS sign for acute appendicitis
Patient lying supine, provider places hand just above right knee and has patient lift leg against resistance.
Describe the Obturator Sign for acute appendicitis
Internally rotate right thigh, with flexed knee
Describe imaging for acute appendicitis
1) CT abdomen & pelvis preferred (IV contrast recommended)
2) U/S focused in RLQ preferred for pregnancy & children
3) MRI abdomen for pregnant women & children (cooperative)
4) Plain radiography (xray) not recommended
5) Choice of modality subject to availability of scanner technology
Describe CT scans for acute pancreatitis
1) 95% sensitivity, 96% specificity
2) > 6 mm diameter, thickened wall (>2mm) with enhancement, peri-appendiceal fat stranding, & appendicolith
3) An air-filled appendix on CT essentially excludes acute appendicitis
4) Advantage over U/S: ability to visualize entire abdomen
Describe ultrasounds for acute appendicitis
1) 85% sensitivity, 90% specificity
2) No radiation; no IV contrast; can be done at bedside
3) Lower diagnostic accuracy than CT or MRI
+ findings: Non-compressible, double wall thickness > 6 mm, focal pain over appendix with compression, appendicolith, peri appendiceal fat, fluid in RLQ
4) Limited use in morbid obesity, perforation, or retrocecal position
What is important to differentiate before you treat acute appendicitis?
Non-perforated (aka, simple or uncomplicated) vs perforated
Describe how to Tx non-complicated/ non-perforated appendicitis
1) IV pain control, NPO, IVF
2) Timely appendectomy: treatment of choice (major goal is prevention of perforation)
-Laparoscopic appendectomy is procedure of choice for uncomplicated cases
-Open – rarely done any more
3) IV Antibiotics- if not immediate (or any) operation planned
4) Interventional radiology: CT-guided drainage & IV antibiotics for abscess found on imaging; appendectomy follows
Describe how to Tx complicated/ perforated appendicitis
1) Emergency appendectomy, may need:
2) Interventional radiology: CT-guided drainage & IV antibiotics for abscess found on imaging; appendectomy follows
True or false: there are various non-pathologic locations for the appendix
True
