Gastroenterology Flashcards
What anatomical landmark is used to classify upper vs lower GI bleeds?
Ligament of Treitz
What are the causes of UGIB?
Above the GE junction
- Esophageal varices (cirrhosis)
- Esophagitis
- Esophageal cancer
- Mallory-Weiss tear
- Boerhaave’s syndrome
Stomach
- Gastric/Peptic ulcer disease – Most common w/ NSAID and H. pylori
- Gastritis – one of most common cause of UGIB (common with EtOH use)
- Gastric cancer
- Dieulafoy lesion
Duodenum
- Ulcer in bulb
- Aorto-enteric fistula: usually only if previous aortic graft
Vascular
- Arteriovenous malformation
- Angiodysplasia
Which investigations should be done for UGIB?
Labs: - CBCd, lytes, urea, Cr, glucose - INR, PTT, type and screen, cross-match if appropriate - AST, ALT, bilirubin, albumin
Radiology/Imaging: 3 views AXR if peritonitis
Invasive Diagnostic Interventions: Endoscopy, ECG
May need wireless endoscopy capsule/ double balloon endoscopy
What percentage of GI bleeds stop spontaneously?
80%
Medical treatment of UGIB?
Medical: restore fluids, PPIs to reduce rebleed, can stabilize clots, if urgent start IV then oral. Use PPI pre-endoscopy to reduce endoscopic stigmata and decrease need for endoscopic therapy
Two most common procedures endoscopically for UGIB?
epi injection therapy + thermal
What should you consider to accelerate gastric emptying prior to gastroscopy to remove clots from stomach?
IV erythromycin
Acute treatment of esophageal varices?
IV Octeotride (somatostatin analogue that decreases splanchnic blood flow/portal pressure), endoscopic therapy: variceal ligation or sclerotherapy.
Longterm treatment of esophageal varices?
B-blocker, nitrates, repeat EVL/sclerotherapy
Persistent/recurrent treatment of esophageal varices?
TIPS (transhepatic internal portal shunt – risk is that you bypass blood over liver and lose detox). Blakemore tube
Causes of LGIB?
Diverticular (60% from right colon)
Vascular
- Angiodysplasia (small vascular malformations of the gut)
- Anorectal (hemorrhoids, fissures)
Neoplasm: cancer, polyps
Inflammation: Colitis (ulcerative, infectious, radiation, ischemic)
Post-polypectomy
What type of bleeding for LGIB results in unchanged bowel habits?
Anal bleeding
What is angiodysplasia?
Vascular malformation (focal submucosal venous dilatation or tortuosity)
Physical for Rectal Bleeding/Altered Bowel Habit?
Abdo exam EDAP (External, digital, anoscopy, proctoscopy)
Investigations for LGIB?
● >50yo + bleeding > colonoscopy (if with red flags urgently)
● <50yo + bleeding > rigid or flexible sigmoidoscopy/barium enema
If LGIB and you have increased suspicion of UGIB what should you order?
colonoscopy + gastroscopy
For slow LGIB investigations?
For SLOW bleeding (<0.5mL/min) > Radionucleotide Tc-99m-tagged RBC scan
For rapid LGIB investigation?
For RAPID bleeding (>0.5mL/min) > Angiography ± Embolization
Dysphagia can be thought of in two categories.
Oropharyngeal and esophageal
Symptoms of oropharyngeal dysphagia
Nasal regurg, difficulty initiating swallow, choking/coughing. Perhaps some associated neuro symptoms
3 broad causes of oropharyngeal dysphagia?
- Neurological
- Muscular
- Structural
Neurological causes of oropharyngeal dysphagia?
MS, stroke
Muscular causes of oropharyngeal dysphagia?
polymyositis, myasthenia gravis, muscular dystrophy
Structural causes of oropharyngeal dysphagia?
Zenker’s diverticulum, thyromegaly/goiter, cervical spur, tumor
Investigations for oropharyngeal dysphagia?
Neurological exam + Cine swallow
Esophageal dysphagia can be broken up into.
Mechanical and motor
Mechanical obstruction primarily affects solids or liquids
Solids
Motor dysphagia primarily affects solids or liquids
Both
Examples of intermittent mechanical dysphagia
Lower esophageal rings/webs - Schatski’s ring
Symptoms of mechanical dysphagia?
SOLIDS worse than liquids. Not temp sensitive, regurg of boluses
Examples of progressive mechanical dysphagia
If age >50 and associated weight loss - cancer. If heartburn associated peptic stricture
Investigations for mechanical causes of dysphagia.
Barium swallow, endoscopy (+/- biopsy)
Symptoms of motor dysphagia
Gradual onset, liquids and solids both affected, temp sensitive
Examples of intermittent motor dysphagia
Diffuse esophageal spasm
What symptom/s would make you think of diffuse esophageal spasm.
Spontaneous chest pain that radiates to the back + GER
Triad for achalasia
Weight loss, regurg undigested food and dysphagia
Examples of progressive motor dysphagia
Achalasia, scleroderma (reflex symptoms)
Investigations for motor dysphagia
Barium swallow, esophageal manometry
Classic bird’s beak narrowing
Achalasia
Which enzymes are indicators of hepatocyte damage?
ALT and AST
Which enzymes are indicators for bile duct damage?
ALP and GGT
Which liver enzyme is more specific to liver damage?
ALT
What is the most common cause of increased ALT?
Fatty liver
What can increase an AST?
Liver damage, kidney, brain, RBC and muscle (rhabdomyolysis, MI, extensive surgery, PE)
DDx for increased ALT/AST
DINA-MAVO
Drugs - anabolic steroids, tylenol, amox/clav
Infection - viral hep
Non-alcoholic fatty liver - associated with features of metabolic syndrome
Alcohol - AST>ALT, increased MCV, increased GGT, increased IgA
Metabolic liver disease - Wilsons, A-1 antitrypsin deficiency, hemochromatosis
Autoimmune
Vascular liver disease - ischemic hepatitis, budd chiari
Other - Neoplastic (HCC, mets)
AST/ALT ratio of <1
Viral or autoimmune hepatitis (chronic liver disease)
AST/ALT ratio of >2
EtOH liver disease or biliary obstruction
AST/ALT ratio of >4
Wilson’s Disease
What do you use to assess biliary function?
Serum bilirubin, serum albumin, ALP, GGT
If bile and pancreatic lipases are unable to reach the bowel because of a blockage (e.g. in obstructive post-hepatic pathology), fat is not able to be absorbed, resulting in stools appearing
Pale, bulky and more difficult to flush.
Examples of unconjugated hyperbilirubinemia
Haemolysis (e.g. haemolytic anaemia)
Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)
Impaired conjugation (e.g. Gilbert’s syndrome)
Examples of conjugated hyperbilirubinemia
Hepatocellular injury
Cholestasis
Causes of increased ALP?
Cholestasis, bone growth (Paget’s disease, osteoblastic cancers – breast) placenta , anabolic steroids
A raised ALP in the absence of a raised GGT should raise your suspicion of non-hepatobiliary pathology. Causes of an isolated rise in ALP include
- Bony metastases or primary bone tumours (e.g. sarcoma)
- Vitamin D deficiency
- Recent bone fractures
- Renal osteodystrophy
What to use to assess liver synthetic function (the last two things to go)?
PT and serum blood glucose
Common causes of large duct cholestasis
- Benign (stricture, stones, primary sclerosing cholangitis (MOST COMMON)),
- Malignant (GB ca, ampullary ca, pancreatic ca)
Common causes of small duct cholestasis
- Granulatomous - DINA (drugs, infection (TB or schistosomiasis), neoplasm (lymphoma), autoimmune (sarcoid, primary biliary cirrhosis or cholangitis).
- Drugs (protease inhibitors, hormones, antibiotics, steroids)
- Other (fibrosing or alcohol hepatitis, rare disorders, amyloid, paraneoplastic)
What is sialadenitis?
Inflammation of the salivary glands
Typical presentation of sialadenitis?
Presentation: acute onset of pain and edema of parotid or submandibular gland that may lead to marked swelling ± fever, ±leukocytosis, ± suppurative drainage from punctum of the gland
Lab features of sialadenitis?
Lab features: high serum amylase
What causes sialadenitis?
Cause: usually bilateral (sometimes unilateral) inflammation of the salivary glands caused by mumps virus (usually Paramyxovirus) OR bacteria (often staph aureus).
Treatment of sialadenitis?
Treatment: supportive if viral. Complications can affect postpubertal male testicles causing epididymitis → sterility. If bacterial – treat with cloxacillin ± abscess drainage, sialogogues
What is the definition of sialolithiasis?
Presence of calculi/stones in salivary glands or ducts
What gland does sialolithiasis usually occur?
Most (80 to 90 percent) salivary gland stones occur in the submandibular glands, 6 to 20 percent occur in the parotid glands, and 1 to 2 percent occur in the sublingual or minor salivary glands
What is the common presentation of sialolithiasis?
Pain in gland region especially when eating ± swelling near submandibular region. About 33% present with painless swelling. Usually unilateral.
Investigations for sialolithiasis?
Can show up on X-ray, but up to 20% not detected on X-ray. Can try sialogram (inject dye and film duct system).
Management of sialolithiasis?
- Mainstay is conservative management - Patients should be instructed to keep well hydrated, apply moist heat to the involved area, massage the gland, and “milk” the duct
- Nonpharmacologic agents that promote salivary flow (eg, tart, hard candies such as lemon drops)
- Discontinue medications with anticholinergic effects that reduce salivary flow, such as diphenhydramine and amitriptyline.
- NSAIDS
- Surgical intervention — If minimally invasive interventions are not successful, the salivary stone can be removed surgically.
Risk factors for xerostomia?
Risk factors for this includes age and medication use
What is xerostomia?
Mouth dryness or mucinous quality saliva
Causes of xerostomia?
Causes: anticholinergic action of systemic medications, radiation for head/neck cancer, Sjogren’s syndrome
Presentation of xerostomia
Presentation: messed up taste, dry mouth or mucous mouth, infection, dental caries (saliva acts as a buffer)
Management of xerostomia?
Management: review meds, dental measures, substitute or stimulate saliva with ACh analogues (e.g. Pilocarpine).
What is Sjogren’s syndrome?
Autoimmune injury to salivary + lacrimal glands (incurable)
What are the most common diseases associated with secondary Sjogren’s?
The most common diseases associated with SS are rheumatoid arthritis and systemic lupus erythematosus.
What is presentation of sicca syndrome?
Presentation: dry eyes and mouth, possible swelling of glands usually bilaterally.
What is the risk of primary Sjogren’s
Malignant lymphoma developing in salivary glands
When should Sjogren’s syndrome be suspected
In individuals with persistent symptoms of dry eyes and/or mouth, parotid gland enlargement, an unexplained increase in dental caries, or abnormal results of specific serologic tests (eg, anti-Ro/SSA antibodies with or without anti-La/SSB antibodies, rheumatoid factor, and hyperglobulinemia).
Treatment of Sjogren’s syndrome?
Incurable, maybe monoclonal antibodies, saliva substitutes or stimulants (Salagen)
What is a mucocoele?
They are cavities filled in with mucus and lined by epithelium or covered by granulation tissue, resulting from damage of a salivary gland duct and extravasation of mucus into the surrounding tissue.
Presentation of mucocoele?
Presentation: Hx: minor trauma, esp. lower lip usually in young children and adults
What is the standard management of mucocele?
Remove associated minor gland. Surgical removal of the entire lesion and histologic confirmation of clinical diagnosis is the standard management of mucocele
What treatment option should not be done for mucoceles?
No Tx with lancing
What causes cheilitis?
Excess sun exposure. It can also be a sign of iron deficiency.
What is cheilitis?
Cheilitis is an acute or chronic inflammation of the lips characterized by dryness, scaling, erythema, and fissuring of the lips.
Before making the diagnosis of burning mouth syndrome, what should you exclude
Exclude other mucosal diseases, including xerostomia and allergic contact stomatitis.
What is burning mouth syndrome and who does it primarily affect?
Burning mouth syndrome is a disorder affecting predominantly postmenopausal women characterized by a persistent intraoral burning sensation, without clinical signs, and for which no medical or dental cause can be found.
Treatments for burning mouth syndrome?
Treatments for burning mouth syndrome include tricyclic antidepressants, benzodiazepines, and gabapentin.
Most common gland for salivary gland neoplasm?
Cause: esp. parotid gland (80-85%) but majority benign
What percentage of minor salivary gland tumors are malignant?
> 50% minor salivary gland tumors are malignant
Treatment of minor salivary gland tumors?
Tx: wide excision
What is the most common cause of mouth ulcers.
Recurrent aphthous stomatitis
What are aphthous stomatitis (Canker sores)?
Aphthae are painful oral lesions that appear as localized, shallow, round to oval ulcers with a yellowish adherent exudate centrally.
What causes aphthous stomatitis (Canker sores)?
Causes: Many patients with RAS experience an exacerbation of their disease following trauma to the oral mucosa, such as biting the inside of the cheek or undergoing a dental procedure.
In most individuals when do aphthous stomatitis (Canker sores) resolve?
In most individuals, they resolve in 10 to 14 days
List three associated conditions of aphthous stomatitis (Canker sores).
Celiac + crohn’s, behcet’s syndrome (Triad of oral, genital, and eye ulcers)
Behcet’s Syndrome triad
Triad of oral, genital, and eye ulcers
Behçet syndrome is believed to be due to ____?
Behçet syndrome are believed to be due to vasculitis. Among the systemic vasculitides, Behçet syndrome is remarkable for its ability to involve blood vessels of all sizes (small, medium, and large) on both the arterial and venous sides of the circulation.
_______ the most specific lesion for Behçet syndrome, occurs in 75 percent or more of patients with Behçet syndrome
Genital ulceration, the most specific lesion for Behçet syndrome, occurs in 75 percent or more of patients with Behçet syndrome
______ can be associated with canker sores – other manifestations include candidiasis, hairy leukoplakia, squamous cell carcinoma, Kaposi’s, or major ulcers.
HIV/AIDS can be associated with canker sores – other manifestations include candidiasis, hairy leukoplakia, squamous cell carcinoma, Kaposi’s, or major ulcers.
Treatment for recurrent aphthous stomatitis
Tx: General measures aimed at maintaining good oral hygiene (soft toothbrush, waxed tape-style dental floss, and a soft-tipped gum stimulator to gently remove plaque are generally well tolerated.), avoiding exacerbating factors (reduce traumatic factors inside the mouth (eg, sharp/rough dental restorations, braces). Avoid habits that cause trauma (eg, biting cheeks or lips) and foods that seem to exacerbate the process), and reducing pain (viscous lidocaine) are appropriate for essentially all patients with RAS
Early childhood caries are an infectious disease caused by ____
Early childhood caries are an infectious disease caused by strep mutans
What population/s does early childhood caries affect more?
Affects low income/Aboriginals more
How can you prevent early childhood caries?
Prevention: early identification of disease or risk (enamel is thinner near the gingiva), stop transmission (improve mum’s oral health), lower bacterial levels (screening, brushing, fluoride), reduce enviro factors like diet and bottle feeding at night, apply fluoride to strengthen teeth.
Treatment of early childhood caries?
- Extracted are by expanding the socket, severing the periodontal ligament
- Stainless steel crowns
Risk factors for oral squamous cell carcinoma?
Risk factors: sun exposure, smoking, alcohol
What are considered pre-malignant lesions for oral squamous cell carcinoma?
Pre-malignant lesions (i.e. leukoplakia or erythroplakia)
Appearance of oral squamous cell carcinoma?
Cancers are often indurated and firm with a rolled border.
How often is the oral mucosa involved in lichen planus?
The oral mucosa is involved in about 50% of cases
Appearance of lichen planus (oral) and what are their hallmark feature?
Reticulated, lacy, bluish white, linear lesions (Wickham striae) are a hallmark of oral lichen planus, especially on the buccal mucosae.
What are the two groups for oral cleft?
2 groups:
- Syndromic (30%) - oral clefts are those present in patients with recognized congenital syndromes or with multiple congenital anomalie. Chromosome abnormalities and defined monogenic syndromes.
- Nonsyndromic (70%) - oral clefts are those present in patients without associated anomalies or developmental delays.
Treatment of oral cleft?
Tx: surgical repair
Investigations for abdominal/pelvic mass?
- Labs: CBC (anemia, infection), LFTs, amylase + lipase (pancreatic CA), CEA (colon CA), α-Fetoprotein (HCC), CA-125 (ovarian CA)
- Endoscopy
- ERCP
- US (biliary tree + liver)
- CT (neoplasms + infection)
- MRI (delineate liver masses)
- Leukocyte scans may define the extent and locations of intra-abdominal abscesses
History for abdominal/pelvic mass?
- Pain related to meals or defecation suggests a lumenal origin, whereas gross or occult fecal bleeding or alterations in bowel function suggest either a primary source within or invasion of a lumenal site.
- Nausea and vomiting with abdominal distension raise concern for an obstructive process within the proximal gut.
- Dysuria or hematuria may indicate involvement of the urinary tract either by primary disease or by local irritation, as with Crohn’s disease.
- Jaundice suggests benign or malignant obstruction at the level of the pancreas or bile ducts.
- Impingement of a large mass on surrounding vasculature may present with lower extremity edema or intestinal ischemia.
- Ascites may indicate peritoneal metastases from an intra-abdominal malignancy or a worsening of liver function in a cirrhotic patient with hepatocellular carcinoma.
- High fever points toward an intra-abdominal abscess, whereas unexpected loss of more than 5% of body weight raises suspicion of malignancy
- HTN
- Menstrual irregularities
Physical exam for abdominal/pelvic mass?
- Scleral icterus or jaundice suggests liver infiltration versus biliary obstruction from a bile duct or pancreatic tumor.
- Temperature higher than 38°C is consistent with an infectious or inflammatory process such as an intra-abdominal abscess.
- If the mass is tender, as with Crohn’s disease, this suggests that the mass is inflammatory.
- Lymphadenopathy raises concern for metastatic malignancy. Palpable supraclavicular (Virchow) or periumbilical (Sister Mary Joseph) nodes are found with gastric cancer.
- Rectal examination detects approximately half of all rectal neoplasms
Etiology for abdominal/pelvic mass?
Organomegaly
- Hepatomegaly
- Splenomegaly
- Enlarged kidneys (e.g., cysts, hydronephrosis)
Neoplasms (benign/malignant)
- Lymphoma/Sarcoma
0 Gastrointestinal tumors (e.g., gastric, colon, pancreas, hepatoma, gastrointestinal stromal tumor)
- Gynecologic tumors (e.g., ovarian, uterine)
- Renal/adrenal
- Neuroblastoma
Gynecologic
- Ovary (e.g., benign or malignant)
- Tube (e.g., ectopic pregnancy)
- Uterus (e.g., leiomyoma, pregnancy)
Bladder/prostate (e.g., urinary retention, cancer)
Other
- Pancreatic pseudocyst
- Vascular (abdominal aortic aneurysm)
- Abdominal wall masses
Definition of constipation?
Infrequent passage of stools, passage of hard/small stool, excess straining during defecation or sense of incomplete bowel evacuation
2 categories of aetiologies constipation
- Functional
2. Organic
What are the aetiologies of functional constipation?
Slow-transit constipation (Chronic constipation with modest abdominal discomfort in a patient who has used laxatives for a long time), irritable bowel syndrome, pelvic floor dysfunction (functional defecatory disorders)
What are the aetiologies of organic constipation?
- Medication side effects (narcotics, antidepressants/, Ca channel blockers) are the most common
- Intestinal obstruction, left sided colon cancer (consider in older patients), and fecal impaction
- Metabolic – DM, hypothyroidism, hypercalcemia, hypokalemia, uremia
- Neurological - spinal cord compression/injury, intestinal pseudo-obstruction, Parkinson’s disease, MS
- Collagen vascular disease (e.g. scleroderma)
- Painful anal conditions (e.g. fissures)
- Diet: Low-fiber diet, sugar-restricted diet, chronic laxative abuse
Clinical features of constipation?
Stool firm, difficult to expel, passed with straining, abdominal pain relieved by defecation, flatulence
Red flags of constipation?
Certain findings raise suspicion of a more serious etiology of chronic constipation: Distended, tympanitic abdomen, Vomiting, Blood in stool, Weight loss, Severe constipation of recent onset/worsening in older patients
How to calculate constipation score?
Based on a flat AXR, divide into four quadrants (ascending, transverse, descending, and rectosigmoid colon) – rate the amount of stool in each quadrant 0-3 and a total score of >6/12 suggests constipation
Bristol stool chart
1: like rabbit droppings 2: grapes 3: corn on cob 4: sausage 5: nugs 6: porridge 7: gravy
What investigation should be ordered if concomitant symptoms such as rectal bleeding, weight loss, anemia or age above 50 in constipation?
Colon visualization (colonoscopy, CT colonography)
What physical exam should you do for chronic constipation?
RECTAL EXAM (anal wink reflex, observe perineal descent on bearing down, resting tone, squeeze pressure).
What are the investigations if constipation is the only presenting symptom?
- Underlying disease rarely found if constipation is the only presenting symptom – thus treat symptomatically
- Only test indicated in this situation is a CBC (2013 recommendation of American Gastroenterology Association), but also consider TSH, calcium, and glucose, X-ray of abdomen
If therapeutic trial does not work for constipation what should be your next steps?
Send for colonic transit or anorectal manometry if normal, or barium/MR defecography in unsure. NO COLONOSCOPY unless >50 or alarm features.
What are the examples of surfactants in the treatment of constipation and how do they work?
Stool softeners such as docusate sodium 100-240mg PO QID (eg, Colace) are intended to lower the surface tension of stool, thereby allowing water to more easily enter the stool. Although these agents have few side effects, they are less effective than other laxatives
What is the patient education and dietary changes to recommend in the treatment of constipation?
o Patient education: exercise, hydration of 8-10 glasses per day) + stop offending meds + treat underlying cause
o Dietary changes and bulk-forming laxatives: Dietary fiber (wheat bran/high fibre cereals) and bulk-forming laxatives such as psyllium or methylcellulose 2-3 teaspoon/day
What are the examples of osmotic agents in the treatment of constipation and how do they work?
PEG – PEG 3350 250ml-4L PO PRN and powdered preparations (eg, MiraLAX) that do not contain electrolytes are available for the treatment of chronic constipation
Synthetic disaccharides – Lactulose 15-60ml PO daily (eg, Enulose) is a synthetic disaccharide. It is not metabolized by intestinal enzymes; thus, water and electrolytes remain within the intestinal lumen due to the osmotic effect of the undigested sugar. Lactulose requires some time (24 to 48 hours) to achieve its effect. Another example is Sorbitol 15-30ml PO BID
Saline – Saline laxatives such as milk of magnesia 15-30ml PO BID, magnesium citrate 150-300ml PO daily, or water containing high amounts of magnesium sulfate are poorly absorbed and act as hyperosmolar solutions
What are the examples of stimulant agents in the treatment of constipation and how do they work?
Stimulant laxatives such as bisacodyl (eg, some forms of Dulcolax), senna (eg, Senokot), and sodium picosulfate (eg, Dulcolax drops) primarily exert their effects via alteration of electrolyte transport by the intestinal mucosa. They also increase intestinal motor activity.
What is the treatment for severe constipation?
- Initial trial of suppositories (glycerin or bisacodyl) since suppositories can be effective in liquifying stool and thereby overcoming obstructive defecation.
- Disimpaction — Patients with a fecal impaction (a solid immobile bulk of stool in the rectum) should initially be disimpacted starting with manual fragmentation if necessary. After this is accomplished, an enema with mineral oil will help to soften the stool and provide lubrication.
What is the definition of diarrhea?
Increased stool liquidity + weight (more than 300 g/day), increased stool frequency (>3/day)
What are the symptoms of diarrhea?
Associated with urgency, abdominal cramps, and incontinence
What is the definition of acute diarrhea and when does it resolve?
(<2 wks) is usually infectious (90%), a drug side effect, or a toxin. Usually self-limiting + resolve within 7d.
Risk factors for acute diarrhea?
Raw or undercooked meat/seafood, unpasteurized dairy products, antibiotics/laxatives, high risk sexual activity, infectious outbreaks, family history (IBD), occupational exposures
Acute diarrhea can be broken up into 2 types?
- Non-inflammatory (Watery)
- Inflammatory
Etiology of non-inflammatory (watery) acute diarrhea?
Viral (Rotovirus, Adenovirus, Norovirus), E Coli, Giardia, Cryptosporidiosis (Every virus gets caught), drugs (colchicine, antibiotics):
• Rotavirus (MOST COMMON for kids) – oral-fecal transmission, contagious, diagnose by stool antigen test. NEW VACCINE AVAILABLE (LIVE).
• Adenovirus is similar but can be transmitted by the respiratory route.
• Norovirus – oral-fecal also, from shellfish, often associated with vomiting. ON CRUISES! Cooking kills it
Symptoms of inflammatory acute diarrhea?
Bloody (not always), Small volume, high frequency, Often lower abdominal cramping with urgency ± tenesmus. May have fever ± shock
Investigations for inflammatory acute diarrhea?
Fecal WBC and RBC positive
Pathophysiology of inflammatory acute diarrhea and what part of the bowel does it affect?
- Organisms and cytotoxins invade mucosa, killing mucosal cells, and further perpetuating the diarrhea
- Usually colon
Etiology of inflammatory acute diarrhea?
Salmonella, Shigella, Campylobacter – most common, E Coli 0157H:7, Yersinia. (SECSY). Others: NSAIDs, IBD, ischemic
What is the definition of chronic diarrhea?
> 4wks, rarely infectious/parasitic (exceptions are Giardiasis, C. Difficile)
What are the 4 categories of chronic diarrhea?
- Osmotic
- Secretory
- Inflammatory
- Abnormal motility
Pathophysiology of osmotic chronic diarrhea?
Caused by ingestion of non-absorbable, osmotically active substance. Usually lactase would cleave lactose into component sugars, but if deficient, then lactose continues into colon where bacteria will digest and cause CO2/H2 production (fermentation) + short-chain-fatty-acids = liquidy stool
Etiology of osmotic chronic diarrhea?
Congenital vs. acquired due to viral gastroenteritis, small bowel disease – celiac or Crohn’s, aging. Lactose, fructose, mannitol/sorbitol, lactulose, divalent ions Mg2+ ingestion – antacids or Epsom salts.
S&S of osmotic chronic diarrhea?
Diarrhea stops with fasting, Hx of ingestion of offending substance, minimal cramps and pain - no RBC’s or mucus in stool; stool pH<6 if carbohydrate malabsorption
Pathophysiology of secretory chronic diarrhea?
Loss of fluids + electrolytes from intestine
Etiology of secretory chronic diarrhea?
Cholera, meds (Mg antacids, Abx, NSAIDs, colchicine, beta blockers, PPI, antineoplastic agents, prostaglandins), bacterial toxins, bile salt wasting (prev. cholecystectomy), toxins (EtOH, arsenic), secretagogues, laxatives
S&S of secretory chronic diarrhea?
Diarrhea persists despite fasting, minimal cramps and pain, large volume watery stools, absence of mucus, blood, or excess fat in the stool
Pathophysiology of inflammatory chronic diarrhea?
Some kind of damage to gut villi = breakdown of cells = activated inflammatory mediators
Etiology of inflammatory chronic diarrhea?
Invasive infections (Salmonella, Shigella, E.coli 0157H:7, Campylobacter, Yersinia), radiation therapy, IBD (UC or Crohn’s)
S&S of inflammatory chronic diarrhea?
Systemic symptoms like fever, fatigue, night sweats, weight loss; visible blood in stools, significant cramps and pain, PMN’s on stool microscopy
Pathophysiology of abnormal motility chronic diarrhea?
Reduced transit time leads to decreased water absorption.
Etiology of abnormal motility chronic diarrhea?
IBS, hyperthyroidism, post-surgical diarrhea (vagotomy, resection of ileocecal valve)
S&S of abnormal motility chronic diarrhea?
Stools tend to be soft, porridge-like
Compare organic vs functional diarrhea
o Organic: systemic features, blood, pus, weight loss, nocturnal diarrhea, recent onset, age >50.
o IBS/functional: no systemic features, no blood or pus, stable weight, never at night, longstanding, age <50.
What causes traveller’s diarrhea and how can it be prevented?
Can be due to bacteria (E coli – most common, salmonella, C jejuni), virus (rotavirus), or parasite (giardia from Nepal, St Petersburg, Rocky Mountains). Prevent through normal measures and prophylaxis (Dukoral for E coli and Cholera – only 40% effective for 3 mnths).
What are you concerned about if prior antibiotic use for etiology of diarrhea?
C Difficile (get pseudomembranous colitis)!
What are you concerned about if HIV for etiology diarrhea?
Opportunistic infections (Cryptosporidia, CMV)or lymphoma
History for diarrhea?
Travel, homosexual contacts, outbreaks, seafood, extraintestinal signs of IBD, FHx, antibiotics, diet, steatorrhea, weight loss, immunosuppressed, laxatives, tumor history , sexual history
Investigations for acute diarrhea?
Stool culture/microscopy (C&S/O&P) required for inflammatory/severe/epidemiological purpose
- C&S: only tests Salmonella, Shigella, E.coli 0157H:7, Campylobacter; must order other organism
- C. Difficile Toxin: if recent/remote abx use, hospitalization, nursing home, recent chemo
- Flexible Sigmoidoscopy: if not perforation, if inflammatory; biopsies help dx IBD vs. infectious colitis
Investigations for chronic diarrhea?
- Stool Analysis for: C. Difficile, C&S/O&P +/- fecal fat, WBC, stool osmolality (secretory vs. osmotic diarrhea)
- Hematology: CBC + lytes + CRP + TSH + celiac serology (IgA, anti-tTG, + IgA = rule out IgA deficiency - ^frequency w/ celiac disease)
- FIT
- Colonoscopy/Ileoscopy/Gastroscopy: If chronic - for biopsy
- Trial: of lactose free diet – however, may delay dx of IBD and celiac disease
DO NOT empirically prescribe anti-diarrheal especially with _______
Fever or hematochezia
Are antibiotics generally required for the treatment of diarrhea?
Generally not required unless pt high risk or has severe Sx (>6 episodes/day, hematochezia, febrile > 1wk)
Most cases are self limiting
First step to management of diarrhea?
Hydration
PO Rehydration Solutions: fluid/lyte replacement PO, IV if severe extremes of age/coma
Pedialyte, Apple Juice, i.e. bring ^Na+ in via Na+ channels + glucose coupled receptors
Antibiotic for C. difficile and duration?
Fidaxomicin or vancomycin. 2nd line - Metronidazole
- Vancomycin is always given IV with C.diff being the one EXCEPTION to it being given orally.
- Duration = 10 days
Antibiotic for Giardia?
Metronidazole
Antibiotic for Salmonella, Campylobacter, E.col?
Cipro
MOA of opioids (antidiarrheal)?
Activation of δ receptors = reduced secretory activity + mew receptors = enhanced NaCl + water absorption = net effect of reduction of fluid entering the large intestines
MOA of absorbants (antidiarrheal)?
Act by absorbing intestinal toxins/micro-organisms or by coating intestinal mucosa
Examples of modifiers of fluid transport (antidiarrheal)?
Bismuth subsalicylate (Pepto-Bismol)
Examples of opioids (antidiarrheal)?
Methylnatrexone or alvimopan. If you constipate someone with too much opioid, reverse with these.
Prevention in Traveler’s diarrhea?
- Food and water choices (boiled or bottled water only, no ice, purify your own water – filter/drops. Avoid: fruit salads, lettuce, chicken salads, guacamole, street vendors. Eat fruit that can be peeled, well cooked, boiled; prophylaxis usually not recommended – but, dukoral PO vaccine (E. Coli, Cholera)
- Empiric Antibiotics for Traveler’s Diarrhea of Moderate/Severe Quality: ciprofloxacin or azithromycin or rifaximin; however, there is increasing fluoroquinolone resistance in causative agents, especially in South America and Southeast Asia
Examples of absorbants (antidiarrheal)?
Kaolin/pectin (Kaopectate), methylcellulose, activated attapulgite
Side effects of anti-motility agents?
Side Effects: abdo cramps, toxic megacolon
Examples of anti-motility agents?
Diphenoxylate, loperamide (Imodium)
Contraindications to anti-motility agents?
Not in mucosal inflammation or hematochezia because of concerns that antimotility agents can prolong disease in such infections or lead to more severe illness. In such patients, bismuth salicylate (Pepto-Bismol, 30 mL or two tablets every 30 minutes for eight doses) is an acceptable alternative
4 types of antidiarrheal?
- Anti-Motility Agents
- Absorbants
- Modifiers of Fluid Transport
- Opioids
What is GERD?
Involuntary reflux of gastric contents into esophagus. The esophagus mucosa has stratified squamous epithelium and is more susceptible to acid damage. The lower esophageal sphincter (LES) blocks acid from coming up into the esophagus. When pressure decreases, gastric acid can reach esophagus and decrease the esophagus pH.
What are the causes of GERD?
Obesity (increased abdo pressure), lower esophageal sphincter pressure, decreased esophageal peristalsis, gastric acid hypersecretion (Zollinger-Ellison syndrome), delayed gastric emptying, and overeating
What are the risk factors of GERD?
EtOH, nicotine, obesity, dietary fat, peppermint, meds (narcotics, Ca2+ channel blockers, aspirin and NSAIDS), hormones (estrogen, glucagon)
What are the typical symptoms of GERD?
- Typical Heartburn - sensation of discomfort or burning behind sternum and radiating toward neck, throat, and occasionally the back; typically occurs postprandially.
- Regurgitation - perception of flow of refluxed gastric contents into mouth or hypopharynx
- Less common/atypical symptoms: chest or epigastric pain and/or discomfort, water brash (excessive saliva mixing with stomach acid in throat and mouth), chronic cough, wheezing, burping or hiccups, bloating, hoarseness, sore throat, dysphagia or odynophagia, either of which indicates upper endoscopy
What should be asked on HPI for GERD?
- Effect of symptoms on quality of life including missed work
- Nocturnal symptoms
- Sleep disturbance
- Alcohol use
- Consumption of various foods reported to possibly provoke GERD symptoms such as coffee, chocolate, fatty or fried foods, or spicy foods (based on limited and conflicting evidence)
What medications can cause GERD?
Medications reported to potentially exacerbate or cause symptoms of GERD include: Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), calcium channel blockers, nitroglycerin, nitrate, anticholinergic agents, alpha-adrenergic antagonists, prostaglandins, theophylline, sedatives, antidepressants, sildenafil, albuterol, glucagon, bisphosphonates
Physical exam for GERD?
o Physical exam typically unremarkable
o Atypical signs of GERD may include: Dental erosion, wheezing, sinus or pulmonary problems such as recurrent otitis media or laryngitis
How is GERD diagnosed?
- GERD is usually a presumptive clinical diagnosis based on bothersome presence of heartburn and/or acid regurgitation, and patient response to empiric trial of proton pump inhibitors (PPIs)
- Proton pump inhibitor (PPI) trial consists of administration of any available PPI at appropriate dose once or twice daily for 1-2 weeks to assess treatment response
What are some indications that testing is required for GERD and what are the options?
Indications include alarm symptoms, high risk for Barrett’s (male, age >50, obese, white, tobacco use), inadequate response to PPI trial (4-8wks)
Options include upper endoscopy (might not show anything) and 24hr pH monitoring
• Can determine relationship between reflux and sx
What are some of the alarm symptoms that should be asked on history?
- Dysphagia
- Odynophagia
- Hematemesis, anemia (symptoms may include fatigue, pallor, or dyspnea on exertion), or other signs of upper gastrointestinal bleeding
- Weight loss
- Epigastric mass
- Vomiting
____ is indicated in patients who have a normal gastroscopy but with chest pain and/or dysphagia?
Esophageal manometry
What is the Ddx for GERD?
Nonmalignant esophageal disorders: Motility disorders such as achalasia or diffuse esophageal spasm, Eosinophilic esophagitis (in adults or children), Other causes of esophagitis, such as pills, infection, radiation, or caustic agents, Rumination syndrome, Esophageal strictures, webs, or rings, Zenker diverticulum
Other nonmalignant gastrointestinal disorders: Functional dyspepsia, Peptic ulcer disease, Gastroparesis, Biliary tract disease or colic, Supragastric belching
Malignancies: Esophageal and esophagogastric junction cancer, Gastric cancer
Coronary artery disease
Chest wall pain
Oropharyngeal and laryngeal disorders
Food allergy
Functional esophageal disorders
_______ which may account for up to 90% of patients reporting heartburn refractory to twice-daily proton pump inhibitors
Functional esophageal disorders
What is functional heartburn?
Reflux hypersensitivity, characterized by normal esophageal acid exposure but a positive (> 95%) symptom association probability (SAP) for acid reflux or nonacid reflux.
Complications of GERD?
Esophageal complications include esophagitis, esophageal ulcer, esophageal stricture, and Barrett’s syndrome. Extra esophageal complications include asthma, aspiration, chronic cough, hoarseness, chronic laryngitis, and dental erosions.
What are the lifestyle treatment options for GERD?
Dietary (avoid fat, caffeine), avoid eating 4h before bed, smoking, elevate head of bed (6-9 in), weight loss, avoid tight fitting clothes.
What are the medical treatment options for GERD?
PPI (pantoprazole) for 4-8 weeks is first line treatment – if inadequate: optimize dose, consider twice daily, consider endoscopy
Histamine receptor antagonist - H2RAs (ranitidine - Zantac) may improve GERD symptoms but may be less effective than PPIs
OTC Antacids PRN may provide short-term relief from heartburn but may not provide prolonged symptom relief nor prevent GERD complications
What are the surgical options for GERD?
Surgery: Nissen fundoplication – gastric fundus is wrapped around the LES strengthening junction
What is the definition of Barrett’s esophagus?
Metaplasia of normal squamous esophageal epithelium to intestinal columnar epithelium containing- type intestinal mucosa (intestinal metaplasia)
Etiology of Barrett’s esophagus?
Thought to be acquired via long-standing GERD and consequent damage to squamous epithelium
Barrett’s esophagus is more common in who?
More common in males, age >50, Caucasians, smokers, overweight, hiatus hernia, and long history of reflux symptoms
Diagnosis of Barrett’s esophagus?
o Endoscopy shows erythematous epithelium in distal esophagus; diagnosis of BE relies on biopsy demonstrating the presence of specialized intestinal epithelium of any length within the esophagus
o BE predisposes first to premalignant changes characterized a slow or high-grade dysplasia, which then progresses to adenocarcinoma
Treatment of Barrett’s esophagus?
o Acid suppressive therapy with high-dose PPI indefinitely (or surgical fundoplication)
o Surveillance gastroscopy every 3yr if no dysplasia
Treatment if high grade dysplasia (Barrett’s esophagus)?
Regular and frequent surveillance with intensive biopsy, endoscopic ablation/ resection, or esophagectomy produce similar outcomes; however, evidence increasingly favouring endoscopic ablation with mucosal resection or radiofrequency ablation
Treatment if low grade dysplasia (Barrett’s esophagus)?
If low grade dysplasia, both surveillance (every 6mo for 1yr then annually) and endoscopic ablation/resection are satisfactory options
Worrisome features of anorectal pain?
Blood in stool, passage of dark blood/clots, recent changes in bowel habits, tenesmus, changes in weight/appetite/energy, personal medical history of polyps, FHx of colon cancer or hereditary polyposis
Physical for rectal bleeding/altered bowel habit?
- Abdo exam
- EDAP (External, digital, anoscopy, proctoscopy)
- External – skin tags, hemorrhoids, fissure, prolapse, skin tags, pruritis, inflammation
- Digital – tone (circumferential), masses, irregularities and tenderness. DON’T DO THIS IF FISSURE
- Anoscopy – best tool for hemorrhoids
- Proctoscopy – looks at the rectum at length
Etiology of rectal bleeding/altered bowel habit?
- If BRBPR and hemodynamic instability > r/o upper GI bleed, diverticular (60% from R colon), meckel’s diverticulum
- Vascular: angiodysplasia, hemorrhoids, fissures
- Neoplasm: CA, polyps
- Inflammation: colitis (UC, infectious, radiation, ischemic)
- Post-Polypectomy
- Trauma
- Coccygeal pain
Investigations of rectal bleeding/altered bowel habit?
- Anoscopy / Rigid Sigmoidoscopy > allow you to see hemorrhoids/rectal mucosa/polyps/CA
- FIT Test > good for occult blood, NOT overt bleeding (screening test)
- To exclude CA:
- > 50yo + bleeding > colonoscopy (if with red flags urgently)
- <50yo + bleeding > rigid or flexible sigmoidoscopy/barium enema
Signs and symptoms of IBD as anorectal pain?
Purulent discharge, Pain in the rectum (sometimes) and/or abdomen (often), Sometimes draining fistula, Sometimes diarrhea
Risk factors of hemorrhoids?
^intra-abdominal pressure (chronic constipation, pregnancy, obesity, portal HTN, heavy lifting)
Etiology of hemorrhoids?
- Vascular and connective tissue complexes form a plexus of dilated veins (cushion)
- Internal: superior hemorrhoidal veins, above dentate line, portal circulation
- External: inferior hemorrhoidal veins, below dentate line, systemic circulation
Internal hemorrhoids symptoms?
Engorged vascular cushions usually at 3, 7, 11 o’clock positions (patient in lithotomy position). Painless rectal bleeding, anemia, prolapse, mucus discharge, pruritus, burning pain, and rectal fullness
What is 1st degree internal hemorrhoid?
1st Degree: bleed but do not prolapse through anus
Treatment for 1st degree internal hemorrhoid
High fibre/bulk diet, sitz bath, steroid cream, pramoxine (Anusol, hydrocortisone, preparation H), rubber bad ligation, sclerotherapy, photocoagulation
What is 2nd degree internal hemorrhoid?
2nd Degree: bleed, prolapse with straining, spontaneous reduction