FINAL - GI Flashcards
When does colon cancer screening begin?
- At age 50 for average risk people
- If personal history of adenoma or significant family history (one FDR with CRC <60, or 2 FDR with CRC ever), start at 40 or 10 years before age of diagnosis of youngest FDR with CRC
How do we screen for colon cancer?
- FIT (fecal immunochemical test) q2 years for average risk individuals
- Colonoscopy (q5 years if family history; if personal hx of precancerous lesion, frequency depends on whether the lesion was high or low risk and how many lesions were removed; ranges from 6mo (high risk precancerous lesion removed in piecemeal fashion) to 10 years (1-4 low risk precancerous lesions removed, no family history)
What happens if someone has an abnormal FIT?
- Colonoscopy
John, 51 yo M, has become your patient today. He has not had a provider for the past 3 years. He reports abdominal pain and 15lbs weight loss x3 months. For colon cancer screening, what would you recommend?
- Colonoscopy (no longer asymptomatic), referral to GI
Karen, age 47, mom and dad with CRC at ages 74 and 85. How to screen for CRC?
Refer to colonoscopy (able to access as of age 40)
Jude, age 35, has a brother with CRC (age 46) and dad with CRC (age 89). How to screen for CRC?
- Refer to colonoscopy at age 36 (ten years younger than age of diagnosis of patients youngest FDR)
Lauren, age 50, history of ulcerative colitis. How to screen for CRC?
- Fit not recommended. IBD increases risk for CRC. Guidelines state “Routine FIT screening is NOT recommended. Refer for ongoing follow-up with a specialist”.
Gertrude, age 86, negative FIT 10 years ago. How to screen for CRC?
- Routine FIT not recommended for age 85+
Rudy, age 76, negative FIT 3 years ago. How to screen for CRC?
- For ages 75-84, assess patient risk of CRC and risk of colonoscopy; harm can outweigh clinical judgement.
Ben, age 58, normal colonoscopy 6 years ago. How to screen for CRC?
- Routine FIT not recommended, patient is up to date with colon screening (q10 years colonoscopy if average risk)
Carol, age 51, wondering about health checks she should have done. How to screen for CRC, assuming average risk?
- FIT q2 year
What are symptoms of CRC to be aware of when deciding whether to send a patient for CRC screening vs. diagnostic colonoscopy?
- Anemia
- Abdominal pain
- Rectal bleeding
- Changes in bowel habits
What is the golden standard to detect and prevent CRC?
- Colonoscopy
What are the pros of colonoscopy?
- High sensitivity and specificity
- Allows for immediate biopsy and polypectomy
- Examines entire colon
- Longer interval between screening
What are the cons of colonoscopy?
- Requires thorough bowel preparation
- Usually requires sedation to minimize discomfort
- Risk of serious complications (perforation)
- Accuracy and complication rate depends on expertise of endoscopist and adequacy of preparation
- Access, cost
What is flexible sigmoidoscopy? What are the pros and cons?
- Examines the rectum and sigmoid colon only
- Can be done without sedation (usually), allows for immediate biopsy and polypectomy, may reduce CRC incidence and mortality
- Still requires some colon prep, does not examine proximal colon, distal lesions require full colonoscopy, still has risk of perf (albeit less so)
A healthy adult liver typically weighs 1.5 kg. How much can the liver weigh when cirrhosis occurs?
Up to 10 kg or more.
Define Non-alcoholic fatty liver disease (NAFLD)
What sub classifications of this disease occur?
= a spectrum of disease, resulting from fat deposition in the liver.
characterized by macrovesicular hepatic steatosis, sometimes with
infammation and/or fibrosis
UNRELATED TO ALCOHOL OR VIRAL CAUSES
Least severe to most severe forms:
1) Steatosis
2) Steatohepatitis
3) Fibrosis
4) Cirrhosis
Distinguish NAFL from NASH
NAFLD is divided into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH)
NAFL: hepatis steatosis without significant inflammation
NASH: hepatic steatosis with hepatic inflammation
Major risk factors/causes of NAFLD
- Typically affects people with metabolic syndrome: central obesity, T2DM, dyslipidemia, HTN
Less common causes: medications (tamoxifen, corticosteroids, MTX), Wilson’s, TPN, rapid weight loss
Patho of NAFLD?
What are some less common causes?
Unclear, mostly attributed to insulin resistance leading to hepatic steatosis
First have fat deposition, then inflammation. Chronic inflammation leads to fibrosis.
Architecture of the liver changes to where it is then classified as cirrhosis.
- histological changes indistinguishable from those of alcoholic hepatitis despite negligible history of
EtOH consumption
S&S of NAFLD
Most patients are asymptomatic (even in late stages)
Some report fatigue, malaise, vague RUQ abdo discomfort
May have hepatomegaly once significant damage. May be accompanied by jaundice, pain, ascites
How is NAFLD usually discovered?
Most often noticed when LFTs are elevated or incidentally on abdominal imaging
4 General diagnostic criteria for NAFLD? (not specific lab findings)
1) demonstration of hepatic steatosis by imaging or biopsy
2) exclusion of significant alcohol consumption
3) exclusion of other causes of hepatic steatosis
4) absence of chronic liver disease
What’s our go to imaging for investigating NAFLD?
U/S
Fibroscan is a special ultrasound technology that measures liver stiffness (hardness) and fatty changes in your liver
CT or MRI will also show fatty infiltrates
There are 3 names for calculations we can do to estimate fibrosis in the liver. DO you know their names?
(probably handy for clinical practice!)
FIB4, NAFLD fbrosis score, Fibrotest
These are calculators that take into account AST, ALT, age, platelet scores, etc
What kind of lab tests will be see elevated in NAFLD? What will you see in the AST/ALT ratio?
Elevated serum AST, ALT, +/- ALP
How does the AST:ALT ratio compare in NAFLD vs alcoholic fatty liver disease?
NAFLD - ratio is lower (<1)
AFLD - AST:ALT >2
What other lab tests do we need to do to r/o alternate causes of hepatitis impairment?
hepatitis A, B and C. Plasma iron, ferritin, TIBC and antibody tests for autoimmune hepatitis
What diagnostic can we use to get a definitive diagnosis of fatty liver?
liver biopsy
liver biopsy cannot distinguish fatty liver from alcoholic vs. non-alcoholic, but considered when
investigating alternative etiologies or assessing for level of fbrosis
T/F
Liver steatosis and steatohepatitis are reversible. Fibrosis and cirrhosis are generally not.
True!
What is the key goal for treatment of fatty liver disease?
Want to reverse factors that contribute to insulin resistance
- healthy diet
- active lifestyle
- gradual weight loss
What rate of weight loss is recommended for NAFLD?
Why not rapid weight loss?
Gradual weight loss (0.5-1kg/wk) - aiming to lose at least 7-10% of body weight – diet and exercise interventions
Rapid weight loss may worsen liver damage
What medications and other measures may be used for treatment of NAFLD?
Abstain from alcohol
Immunization for Hep A and B
Modify risk factors for CVD – optimization of glucose control, treatment of hyperlipidemia, etc
Pioglitazone, liraglutide (balance benefits with adverse effects of weight gain, CHF)
Vitamin E 800 IU daily if hepatic inflammation with non-diabetic, non-cirrhotic patients
Coffee (3 cups/day) and vitamin D
Consideration of bariatric surgery
Prognosis with NAFLD. What usually causes death in people with this condition?
main causes of death, particularly in non-cirrhotic group, are cardiovascular disease and malignancy
- better prognosis than alcoholic hepatitis
■ <25% progress to cirrhosis over a 7-10 yr period - risk of progression increases if inflammation or scarring occurs alongside fat infiltration (nonalcoholic steatohepatitis)
What is cholecystitis?
What is the most common cause?
refers to a syndrome of right upper quadrant pain, fever, and leukocytosis associated with gallbladder inflammation
= Most common complication of gallstone disease
Most common type of gallstones
Cholesterol stones
Patho of cholecystitis?
Inflammation of gallbladder resulting from sustained gallstone impaction neck of the gallbladder
Increased inflammation leads to increased pressure and pain
Possible superimposed infection
No cholelithiasis in 5-10% (typically d/t gallbladder ischemia and stasis) - called acalculous cholecystitis
Who is more likely to get cholecystitis - men or women?
Women
What are the 4 F’s for remembering risk factors of cholecystitis?
Female
Fat (obesity)
Fertile (pregnancy)
Forty (age)
T/F Sudden weight gain is a risk factor for cholecystitis
False
- Sudden starvation or prolonged fasting a risk factor
Which drugs are risk factors for cholecystitis?
- Cholesterol-lowering drugs (known to increase biliary cholesterol saturation)
- Estrogen usage (OCPs and hormone replacement therapy - also increase biliary cholesterol saturation.
- Furosemide.
- Ceftriaxone.
- Cyclosporine.
- Opiate narcotic analgesics.
Which ethnicities have high rates of cholecystitis?
Indigenous, Chinese, or Japanese clients have a high incidence.
Name some other risk factors for cholecystitis (there are so many!)
Total parenteral nutrition (TPN).
Obesity.
Status post bariatric surgery.
Pregnancy secondary to elevated progesterone.
Increasing age.
Haemolytic anaemia.
Diabetes
High serum triglyceride and low high-density lipoprotein (HDL) levels
High-caloric and refined carbohydrate diet.
Cirrhosis, Crohn’s disease, and gallbladder stasis.
Bile acid malabsorption.
What is biliary colic?
How does the pain differ from that of cholecystitis?
Biliary colic = gallstone transiently impacted in cystic duct, no infection
Those with cholecystitis often have hx of biliary colic
Biliary colic is RUQ pain that comes and goes (<6hr), but cholecystitis is a pain which is constant and usually increasing
Where is the pain from cholecystitis felt?
epigastric or RUQ pain
May radiate to right shoulder or back
General S&S of cholecystitis
Epigastric, RUQ pain
Anorexia
N/V
low grade fever (<38.5ºC)
Fat intolerance
Heartburn, upper abdo fullness
Mild jaundice (20%)
Chronic diarrhea
*Acalculous cholecystitis may present with fever and sepsis alone
Often history of ____ ingestion one hour or more before the initial onset of pain
Fatty foods
What focal peritoneal findings might you see on physical exam of a person with cholecystitis? (name specific test)
Murphy’s sign
palpable, and tender gallbladder (in 33%)
Boas’ sign
What is Boas’ sign?
right subscapular pain
Procedure for checking murphy’s sign
patient takes and holds a deep breath while palpating the right subcostal area. If pain occurs when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive
Brief overview of physical exam for cholecystitis.
How might the person present?
Vitals
Typically ill-appearing, febrile, tachycardic, and lie still on the examining table because cholecystitis is associated with true local parietal peritoneal inflammation that is aggravated by movement
Abdo exam - voluntary and involuntary guarding
+ Murphy’s sign
Cardiac exam
Is Murphy’s sign sensitive and/or specific?
highly sensitive (97%)
not specific (48%)
Will lipase be abnormal in cholecystitis?
normal in classic cholecystitis
How sensitive is an U/S for diagnosing cholecystitis.
What scan can we do if U/S is negative?
98% sensitive
HIDA = hepatobiliary iminodiacetic acid scan; is an imaging procedure that uses an injected radioactive tracer and a scanning camera to evaluate the gallbladder
ERCP/MRCP can also show blockage
What other types of labs/testing will be do in suspected cholecysitis?
blood work: elevated WBC and left shift
Bilirubin
Lipase
Alk phos, AST & ALT (should be normal in classic cholecystitis)
Urinalysis to rule out pyelonephritis and renal calculi.
Pregnancy test if childbearing age
Stool guaiac test for occult blood to rule out bleeding
Toronto Notes says the 2 most important labs to do for biliary pain are lipase and bilirubin. Why?
Lipase: to determine if element of pancreatitis
Bilirubin: to determine if there is bile duct obstruction
Treatment of acute cholecysitis
Send to ER
admit, hydrate, NPO, NG tube
Antibiotics, analgesics
Cholecystectomy: early (within 72 hrs) preferred, laparoscopic usually
percutaneous cholecystostomy tube: critically ill or if general anesthetic contraindicated
some centres can perform percutaneous stone extraction to avoid cholecystectomy
What is the most common complication of cholecystitis?
Gangrenous gallbladder (20%) caused by lack of blood supply to gallbladder
Can lead to rupture
What are the physiological functions of the liver?
Synthesize Amino Acids
Synthesize Proteins
Albumin
Immune Proteins
Hormones
Anticoagulants/Clotting Factors
Plasma Proteins (carrier proteins)
Produces Urea
Bile Production: Bile acids (Salts) and Bile Pigment
Regulates CHO metabolism
Control of Cholesterol Metabolism
Sonographic murphy sign =
Abdo tenderness from pressure of ultrasound probe over the gallbladder
Indirect bilirubin = ____________.
Direct bilirubin = _____________.
Only one can be secreted into urine, and can cause bilirubinuria. Which?
Indirect bilirubin = unconjugated
Direct bilirubin = conjugated
Only conjugated can be passed through urine as the conjugation process makes the bilirubin water soluble. This occurs in a hyperbilirubinemia state such as hepatocellular or cholestatic jaundice.
What occurs in chronic cholecysitis
Gallstone dislodges from cystic duct, goes back into gallbladder…over and over
OR
Irritation may also occur just from presence of stones in gallbladder (without actually lodging in ducts)
Leads to gallbladder existing in chronic state of inflammation
Epithelial cell damage and death –> gall bladder mucosa changes and becomes sensitive (pain with each contraction when trying to squeeze out bile) –> fibrosis and calcification of the gallbladder (called “porcelain gallbladder”)
What are some causes of liver damage?
What can liver damage lead to?
Causes of Liver Damage:
Infections
Drugs, toxins
Ischemia (damage to the central lobule)
Autoimmune disorders
Can Lead to:
Hepatocellular Injury
Impaired Biliary Secretion
Necrosis
Fibrosis
Portal Venous Hypertension
Death
How is chronic cholecystitis typically treated?
Likely need cholecystectomy
**high risk of gallbladder CA once has fibrosis and calcification
Which blood tests can indicate liver damage or liver injury? (hepatocellular)
Aminotransferases (AST, ALT)
-Ratio of AST:ALT can hint to certain differentials.
Lactic Dehydrongenase (LDH)
What is choledocholithiasis
= gallstones in the common bile duct
Which is a more specific marker of hepatic injury, ALT or AST?
ALT - remember the L in the middle to remind you of the Liver. (tip from Ruth’s powerpoint) - also found in skeletal and kidney tissue but is more specific to liver
AST is found in a variety of tissues - liver, brain, pancreas, heart, kidneys, skeletal muscles. So you could remember this by thinking of the S as meaning Somewhere else (tip from Gayle’s caffeinated brain)
What are the most common causes of acute pancreatitis?
Gallstones
Alcohol
Other causes (acronym = I GET SMASHED)
Idiopathic
Gallstones (45%)
Ethanol (35%)
Tumours:
Scorpion stings
Microbiological (bacterial, viral, parasites)
Autoimmune
Surgery/trauma
Hyperlipidemia
Emboli or ischemia
Drugs/toxins:
Which LFT blood tests will test for cholestasis?
Bilirubin
GGT
Alkaline Phosphate
5 - nucleotidase (not commonly ordered)
Patho of acute pancreatitis
activation of proteolytic enzymes within pancreatic cells, starting with trypsin, leading to local and systemic inflammatory response
in gallstone pancreatitis, this is due to mechanical obstruction of the pancreatic duct by stones
in ethanol-related pancreatitis, pathogenesis is unknown
Differentiate mild vs severe pancreatitis in terms of the patho
Mild (interstitial) = interstitial edema, peri-pancreatic fat necrosis
Severe (necrotic) = extensive peri-pancreatic and intra-pancreatic fat necrosis
- parenchymal necrosis and hemorrhage → infection in 60%
- release of toxic factors into systemic circulation and peritoneal space (causes multi-organ failure
Which blood tests will test the hepatic synthetic function of the liver?
PT -INR
Albumin
What is Cullen’s sign?
Is it sensitive or specific for pancreatitis?
superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus
sensitive but not specific for acute pancreatitis
What is Grey-Turner’s sign?
What does it mean?
flank ecchymosis
Classically it correlates with severe acute necrotizing pancreatitis, often in association with Cullen’s sign
Typical pain presentation of acute pancreatitis?
epigastric, noncolicky, constant
can radiate to back
may improve when leaning forward (Inglefinger’s sign)
An AST/ALT ratio of less than one (where the ALT is significantly higher than the AST) may indicate _______________________.
Non-alcoholic fatty liver disease.
S&S of acute pancreatitis
- pain
tender rigid abdomen; guarding
N/V
abdominal distention from paralytic ileus
`
fever: chemical, not due to infection
jaundice: compression or obstruction of bile duct
tetany: transient hypocalcemia
hypovolemic shock: can lead to renal failure
acute respiratory distress syndrome
Coma
An AST/ALT ratio equal to one (where the ALT is equal to the AST) may be a sign of acute __________or ________________.
An AST/ALT ratio equal to one (where the ALT is equal to the AST) may be a sign of acute
viral hepatitis
or
drug-related liver toxicity.
An AST/ALT ratio higher than one (where the AST is higher than ALT) may indicate _____________.
Cirrhosis.
An AST/ALT ratio higher than 2:1 (where the AST is more than twice as high as the ALT) is a sign of ____________.
Alcohol-related liver disease.
High or low results on liver functioning tests do not always indicate a health problem.
Factors that may temporarily affect levels of AST or ALT include:
Age
Alcohol consumption
Body mass index
Exercise
Gender
Medications that are toxic to the liver
Pregnancy
Whether or not the patient fasted before the test
Which is more specific for pancreatic damage: amylase or lipase?
Lipase
Diagnostics for acute pancreatitis.
What do we see for each?
increased serum pancreatic enzymes: amylase, lipase
ALT >150 specific for biliary cause
increased WBC, glucose, low calcium
imaging: CT most useful for diagnosis and prognosis
- May also get other imaging to see other organ involvement such as U/S (evaluating biliary tree), x-ray of colon, ERCP, MRCP
Treatment of acute pancreatitis
To the hospital!
goals (only supportive therapy available)
- hemodynamic stability
- analgesia
- oxygen
- stop progression of damage (difficult)
- treat local and systemic complications
What are some blood results you might expect to see if there is hepatocellular injury?
Elevated AST and/or ALT compared to alk. phos.
Bilirubin may be elevated
Synthetic function tests may be abnormal
Prognosis for acute pancreatitis
usually a benign, self-limiting course, single or recurrent
occasionally severe leading to multiorgan failure, shock, death
What is chronic pancreatitis?
= irreversible damage to pancreas characterized by
- pancreatic cell loss (from necrosis)
- inflammation
- fibrosis
Most common cause of chronic pancreatitis?
Etoh
causes a larger proportion (>90%) of chronic pancreatitis than acute pancreatitis
Does lots of bad things to the pancreas
no satisfactory theory to explain why only a minority of individuals with EtOH use disorder develop pancreatitis
Can gallstone cause chronic pancreatitis?
No, only cause acute
What are some blood results you might expect to see if there is cholestasis?
Disproportionate elevation in the alkaline phosphatase compared with the serum aminotransferases
Bilirubin may be elevated
Synthetic function test abnormalities possible (albumin, PT)
Isolated hyperbilirubinemia (ALT & AST are usually normal or only mildly elevated in obstructive jaundice except in the acute phase of biliary obstruction when they can reach > 1000 and then rapidly decrease as cholestatic enzymes rise) - pearl from Ruth’s PP
S&S of chronic pancreatitis
early stages:
- recurrent attacks of severe abdominal pain (upper abdomen and back)
- chronic painless pancreatitis: 10%
late stages: occurs in 15% of patients
- steatorrhea (maldigestion) when >90% of function is lost
- diabetes, calcification, jaundice, weight loss, pseudocyst, ascites, GI bleed
How are the following labs usually seen in chronic pancreatitis?
- Glucose
- ALP
- Amylase and lipase
- stool elastase
increase glucose
increase in serum ALP, less commonly bilirubin (jaundice)
serum amylase and lipase usually normal
stool elastase is low in steatorrhea
What is stool elastase measuring?
A stool elastase test measures the amount of elastase in your stool.
Elastase is one of a few digestive enzymes (“digestive juices”) that your pancreas makes to help digest food
Alk phos can be elevated in pregnancy, or bone mets/recent injuries.
How to tell if an elevated alk phos is related liver?
If GGT is also elevated, the source is likely hepatic.
Order U/S for dilated bile ducts. Refer to GI - as per Ruth’s PP.
Treatment of chronic pancreatitis
most common problem is pain, difficult to control
general management
- complete abstinence from EtOH
- enzyme replacement may help pain by resting pancreas via negative feedback
- analgesics
- celiac ganglion blocks
- time: pain decreases with time as pancreas “burns out”
endoscopy: sphincterotomy, stent if duct dilated, remove stones from pancreatic duct
surgery: drain pancreatic duct, resect pancreas if duct contracted
Steatorrhea
- Pancreatic enzyme replacement
Neither endoscopy nor surgery can improve pancreatic function
This marker is released from the membrane of the epithelial cells of the bile ducts (but also from other sources). In r/t liver investigations, it may indicate cholestatic liver disease.
Alkaline Phosphatase
Blood work results show that this protein is lower than normal, which may indicate nephrotic syndrome, malnutrition, or a protein-losing enteropathy such as IBS.
What is the protein?
Albumin
What can cause a prolonged PT/INR?
Liver disease
Vit K deficiency
Fat malabsorption (leads to Vit K def.)
Pancreatic insufficiency
If your patient was experiencing cholestasis, what would you expect to see in albumin and PT/INR bloodwork?
These would both be normal if there was no hepatocellular involvement.
What conditions is a transabdominal U/S good at picking up?
- Gallstones:
> 2 mm
pericholecystic fluid
impacted stone in gallbladder neck
tenderness when gallbladder is palpated with U/S probe (like a +vs Murphy sign) - Extrahepatic obstruction, indicated by dilated bile ducts
- Focal liver lesions > 1cm diameter. Cysts, solid lesions, carcinoma.
- Diffuse disorders such as cirrhosis and hepatitis, although clinical presentation and BW are better indicators for these.
What is ultrasound elastography used for?
To measure liver stiffness as an index of hepatic fibrosis. Particularly in patients with chronic hep c.
When is a CT of the liver useful?
Very accurate imaging
Identify hepatic masses, particularly small metastases, (accuracy ~80%.)
CT with IV contrast is accurate for diagnosing cavernous hemangiomas of the liver as well as differentiating them from other abdominal masses.
Images not obscured by intestinal gas or obesity.
Detects fatty liver
Detects increased hepatic density that occurs with iron overload.
Less helpful than U/S in identifying biliary obstruction, but often provides the best assessment of the pancreas.
When is a cholescintigraphy useful?
(a compound is given by IV to a fasting patient and the compoundi s taken up by the liver and excreted in bile, then enters the gallbladder)
Helpful in diagnosing acalculous cholecystitis
Detecting bile leaks & anatomic abnormalities
Sphincter of Oddi Dysfunction
Rarely needed to diagnose acute cholecystitis
Is an abdo x-ray recommended when you are investigating the liver?
As per Ruth’s pp:
Not usually useful for Dx of hepatobiliary disorders. Insensitive for gallstones, unless calcified & large. Can detect a porcelain (calcified)
gallbladder. Rarely, in gravely ill patients, x-rays show air in the biliary tree, which suggests emphysematous cholangitis.
MRI is superior to CT or U/S for diagnosing diffuse liver conditions such as fatty liver or hemochromatosis and clarifying focal defects such as hemangiomas.
True or false?
True!
What is an ERCP?
The ERCP procedure diagnoses and treats narrowed or blocked pancreatic or bile ducts. It combines endoscopy and fluoroscopy.
What is the main risk associated with ERCP that you should be aware to watch for?
Increased morbidity.
Morbidity from a diagnostic ERCP with only injection of contrast material is about 1%.
Adding sphincterotomy raises morbidity to 4 to 9% (mainly due to pancreatitis and bleeding).
ERCP with manometry to measure sphincter of Oddi pressure causes pancreatitis in up to 25% of patients.
An serum lipase and/or amylase level elevated 3x more than normal is indicative of?
Acute pancreatitis.
In addition to serum lipase and amylase what are some other markers you might expect to see if someone is experiencing acute pancreatitis?
Leuks
Hematocrit
BUN
hypocalcemia
hyperglycemia
Markers of immune activation:
-CRP
-Interleukin 6, 8 & 10
-Tumor necrosis factor
-PMN elastase
To diagnose acute pancreatitis, you need 2 of these 3 criteria:
- acute onset of persistent, severe, epigastric pain often radiating to the back
- elevation in serum lipase or amylase to three times or greater than the upper limit of normal
- characteristic findings of acute pancreatitis on CT, MRI or U/S
What is the difference between IBS and IBD?
IBS - Irritable bowel syndrome is a bowel condition without underlying physically detectable abnormalities.
IBD - Inflammatory bowel condition involves structural disease of the bowels
What are the two types of IBD?
Crohn’s Disease
Ulcerative colitis
Which part of the bowel does UC affect?
Recurring episodes of inflammation limited to the mucosal layer of the colon. Involves the rectum and may extend proximally and continually
How is UC diagnosed?
Diagnosed based on the presence of diarrhea for more than 4 weeks and evidence of chronic colitis on endoscopy and biopsy.
Other types of colitis need to be excluded through the history, labs and by biopsy.
Most people present with attacks of bloody diarrhea that last weeks to months.
How is the prognosis of UC?
Most patients have intermittent exacerbations alternating with periods of symptom resolution. Complications can include severe bleeding, toxic megacolon, perforation, dysplasia and colorectal cancer . Patients with UC may have a slightly higher mortality compared with the general population
The other type of IBD is Crohn’s disease. What parts of the bowel does this effect?
Transmural inflammation of any portion of the GI tract (from oral cavity to perianal area)
How is CD diagnosed?
Based on radiologic, endoscopic, and/or histologic findings of segmental and transmural inflammation
Prognosis of CD
Variable. Some have continuous and progressive disease, some chronic intermittent symptoms and 20% experience prolonged remission after initial presentation.
IBS is a symptom complex in the absence of an organic cause. What are some diagnostics that should be done to rule out organic cause?
CBC, Ferritin
Age appropriate colorectal cancer
Diarrhea:
Celiac screen
Fecal calprotectin
Infectious diarrhea panel
Constipation:
abdo xray
What are alarm features in patients being worked up for IBS that may prompt further investigation/a scope?
- Onset after age 50
- Rectal bleeding/melena
- Nocturnal symptoms
- Progressive abdo pain
- Unexplained weight loss
- Lab abnormalities (iron deficiency anemia, increased CRP, fecal calprotectin/lactoferrin)
- Family history of IBD or colorectal Ca
After doing initial screening and ensuring no alarm features were present, you diagnose Trevor with IBS. He agrees that he would like to try lifestyle management prior to considering any medication. What do you recommend?
Lifestyle and Dietary Modifications
- Psyllium (soluble fiber) improves both constipation and diarrhea
- Low FODMAP diets
- Possible lactose or gluten avoidance
- Regular meal pattern, avoid large meals
- Reduced intake of fat, insoluble fibers, caffeine and gas-producing foods
- Adequate fluid intake, physical activity
- Stress management: counselling, meditation, yoga
Sally was diagnosed with IBS a few months ago and is still struggling with constipation despite making the lifestyle changes she feels able to make. What pharmacologic options can you offer?
Psyllium up to 12-20g/day as tolerated. Slowly titrate up
Calcium polycarbophil
Magnesium hydroxide
Linaclotide
SSRIs - constipation and abdominal pain treatment
Ralph is wanting to trial medication to help with his IBS, his most troubling feature is abdominal pain. What can we explore for Ralph?
Dicyclomine
Peppermint oil
Hyoscine
Pinaverium, trimebutine
Your last patient of the day, Sarah, has diarrhea predominant IBS. What are her pharm options?
Loperamide
Eluxadoline
Diphenoxylate
TCAs - diarrhea and pain
What is GERD?
Some degree of reflux is normal. Gastroesophageal reflux disease occurs when the reflux of stomach contents causes troublesome symptoms/complications
How does GERD typically present?
Heartburn (pyrosis) and regurgitation.
Other: dysphagia, chest pain, water brash, globus sensation, odynophagia (pain swallowing), extraesophageal symptoms (chronic cough, hoarseness, wheezing), infrequently nausea
T/F: GERD is a clinical diagnosis
True - In patients with classic symptoms, the diagnosis can be made clinically in the absence of alarm features
What are alarm features for GERD that would indicate need for an upper scope?
Alarm features suggestive of a gastrointestinal malignancy (New onset of dyspepsia in patient ≥60 years, Evidence of gastrointestinal bleeding (hematemesis, melena, hematochezia, occult blood in stool), Iron deficiency anemia, Anorexia, Unexplained weight loss, Dysphagia, Odynophagia, Persistent vomiting, Gastrointestinal cancer in a first-degree relative)
Abnormal upper GI tract imaging
Risk factors for Barrett’s esophagus
Patients with suspected GERD who have not responded to an empirical trial of twice-daily proton pump inhibitor (PPI) therapy.
Once you have ruled out red flags, UTD divides the GERD treatment approach into mild and intermittent symptoms and severe/frequent symptoms/ Barrett’s esophagus/erosive esophagitis
What is the approach for mild/intermittent symptoms?
Start 4 week trial of lifestyle/diet modifications, low dose H2RA prn and antacids if symptoms < 1/wk
If symptoms persist, increase to BID H2RA x 2 weeks. If this works and symptoms resolve then go back to lifestyle and PRN H2RA
If symptoms persist, start low dose PPI trial for 4-8 weeks. If this works, taper and discontinue once asymptomatic for 8 weeks.
PPI can be increased to BID if needed.
If symptoms recur after resolution, treat with 8 week course of previously effective med.
What is the treatment approach for GERD this is severe/frequent/ Barrett’s esophagus/erosive esophagitis
Go straight to once daily PPI with lifestyle modifications.
If this does not work after 2 months then can try switching to another drug or increasing to BID x 2 months
Should we aim to wean PPIs off once symptoms resolve?
Yes! after 8 weeks of symptom-free period, unless Barrett’s esophagus
What are lifestyle/diet approaches for management of GERD?
Smoking cessation
weight loss if overweight
elimination of food/drink triggers
Avoid meals 3 hours before bedtime
elevate HOB 4-6 inches
T/F: 70% of peptic ulcers are asymptomatic
True
43-87% of patients with bleeding peptic ulcers present without antecedent dyspepsia or other GI symptoms
What are risk factors for PUD?
NSAID use
h.pylori infection
How is PUD diagnosed?
Definitive diagnosis is done with upper GI scope
All patients with PUD should be tested for H.pylori
What is the disease course of PUD?
60% of peptic ulcers heal spontaneously.
With eradication of H.pylori, healing rates increase to > 90%
Even with continuous PPI use, 5-30% of peptic ulcers recur within the first year - this is based on whether H.pylori has been successfully eradicated.
Outline the treatment for PUD
PPI
Discontinue aspirin/NSAIDs
Treat H.pylori if present
PPI may be required for 4-8 weeks or for maintenance therapy in some situations
Risk factors for hernias
Increased intra-abdominal pressure: obesity, chronic cough, asthma, COPD, pregnancy, constipation, bladder outlet obstruction, ascites, heavy lifting
Congenital abnormality
Previous hernia repair, especially if complicated by wound infection
Loss of tissue strength/elasticity (aging, repetitive stress)
Family history
What is the most common type of hernia?
Indirect inguinal hernia
How do hernias present?
May be asymptomatic, reported as a heaviness or dull sense of discomfort with straining/lifting. If incarcerated or strangulated, may present with N/V, ando pain.
T/F: US evaluation of new hernias is required.
False - in the majority of cases, inguinal or femoral hernias can be diagnosed based upon the physical and history.
US is recommended if intra-abdominal complications are suspected
Another time that US is recommended is if the provider is unable to differentiate the hernia between an inguinal and femoral.
Inguinal hernias can often be managed with watchful waiting. Femoral hernias are higher risk for complications and treatment is usually recommended.
Where are these two types of hernias found?
Femoral hernias present inferior to the inguinal ligament and medial to the femoral artery.
Inguinal hernias present superior to the inguinal ligament
This may be difficult to differentiate, especially in obesity
T/F: Umbilical hernias should be surgically repaired within 3 months of occurance
False, often umbilical hernias can be approached with watchful waiting.
T/F: Daily BMs are normal and necessary for good health
False - daily BMs are not necessarily needed for good health. What is normal varies
Define constipation
Unsatisfactory defecation due to infrequent stools +/-difficult or incomplete stool passage. It is subjective and symptom based.
Patients usually define constipation by its top 3 most bothersome symptoms: straining, hard stools and bloating.
What is the Rome IV criteria for constipation in adults?
When 25% of BMs are associated with ≥2 of the following symptoms, occurring in the previous 3 months with an onset of symptoms >6 months and does not meet criteria for IBS:*
Straining
Hard or lumpy stools
A sense of incomplete evacuation
A sense of anorectal obstruction or blockage
The need for manual maneuvers (e.g. digital evacuation)
< 3 spontaneous BMs per week - Loose stools are not present (including laxative-induced)
Like many things, there are both primary and secondary types of constipation.
What are the three types of primary constipation?
Normal transit (60%) - normal frequency, but stool is hard and/or difficult to pass
Pelvic floor dysfunction (25%) - pelvic floor or external anal sphincter cannot relax. May be accompanied by anal fissures/hemorrhoids.
Slow transit (15%) - infrequent BMs
What are secondary causes of constipation?
Medications, diseases, conditions
ex. cancer/cancer related, hypothyroidism, depression, NSAIDs, opioids, TCAs, b-blockers, many others
What are red flags in constipation?
Age 50 or older with new onset symptoms
Rectal bleeding
Nocturnal symptoms
Significant weight loss
Fever
Anemia
Abnormal physical
Remember lifestyle interventions for constipation as the three F’s
Fibre
Fluid
Fitness/physical activity
RxFiles has a 5 step approach to chronic constipation
Step 1: increase dietary fibre, fluids and physical activity
Step 2: bulk forming laxative (ex. psyllium)
Step 3: add an osmotic laxative (PEG, lactulose, MOM)
Step 4: add PRN glycerin supp, stimulant laxative (senna, bisacodyl) or enema
Step 5: add prucalopride (Restoran) or linaclotide (Constella)
Note there specific approaches on RxFiles for constipation in peds, older adults, pregnant people and opioid-induced constipation
T/F: most cases of acute diarrhea in adults are infectious
True
In which circumstances would it be indicated to do stool testing for an adult with acute diarrhea?
Severe illness (fever ≥38.5°C [101.3°F], hypovolemia, ≥6 unformed stools per 24 hours, severe abdominal pain, or hospitalization)
Features of inflammatory diarrhea (bloody diarrhea, small volume mucous stools, fever)
High-risk host features (age ≥70 years, cardiac disease, immunosuppression, inflammatory bowel disease, pregnancy)
Symptoms persisting >1 week
Public health concerns (eg, diarrheal illness in food handlers, health care workers, and individuals in day care centers)
T/F: Antibiotics are typically recommended for adults with > 4 days of acute diarrhea
False, if non of the above signs then supportive care recommended over empiric antibiotics
What is a risk factor for c-diff that should prompt you to test for it?
Recent antibiotic use or hospitalization
If empiric antibiotic therapy is indicated for acute non-bloody diarrhea, which abx are recommended?
A fluroquinolone or azithromycin
What is the role for loperamide in acute diarrhea?
In non-bloody diarrhea with an absent or low-grade fever, loperamide can be used cautiously for up to 2 days. Do not use if fever, bloody or mucoid stools unless antibiotics are also given (can prolong disease). Bismuth salicylate is an acceptable alternative
What is non-pharm management of acute diarrhea?
Hydration
Dietary modification - may be helpful to avoid fatty foods. Lactose may be difficult to digest for weeks-months.
Encourage boiled starches and veggies
What are the most common causes of chronic diarrhea in adults?
IBS, IBD, malabsorption syndromes (lactose intolerance, celiac disease), chronic infections (especially if immunocompromised)
What are indications for referral to a gastroenterologist for chronic diarrhea?
Alarm features (same as IBS)
Severe diarrhea
Suspected IBD
Inconclusive diagnosis after investigations
Failure to respond to empiric therapy
What initial labs would you send for chronic diarrhea without alarm features?
CBC
TSH/T4
Celiac serology
Serum electrolytes (if severe diarrhea to check for dehydration/abnormalities)
Stool occult blood
Stool test for giardia - once again UTD specifically says giardia. But according to Sarah this should be a more general infectious diarrhea panel.
C-diff if risk factors
Fecal calprotectin (or CRP if fecal calprotectin unavailable)
T/F: if alarm features present, abdominal imaging is required
True
Regarding LFTs, which of these indicate acute liver injury? Chronic? Both?
AST and ALT
PT/INR
Albumin
Acute - AST and ALT (released in hepatocyte inflammation)
Chronic - albumin (half life of about 20 days)
Both acute and chronic - PT/INR - the most sensitive of LFTs
What are some confounders that could mess with a PT/INR result?
Vit K deficiency
Coumadin (warfarin)
Hemophelia
