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
Treatment for 2nd degree internal hemorrhoid
Treatment: rubber band ligation, photocoagulation
What is 3rd degree internal hemorrhoid?
3rd Degree: bleed, prolapse, requires manual reduction
Treatment for 3rd degree internal hemorrhoid
Treatment: rubber band ligation (doesn’t work as well), or hemorrhoidectomy
What is 4th degree internal hemorrhoid?
4th Degree: bleed, permanently prolapsed and cannot be manually reduced
Treatment for 4th degree internal hemorrhoid
Closed hemorrhoidectomy – closes the mucosa with sutures after hemorrhoid tissue removal vs open which leaves the mucosa open. Crohn’s disease is a contraindication to hemorrhoidectomy
Symptoms of external hemorrhoid
Usually present as a bulge or a mass in the anoderm below the dentate line. Often very painful as it is in an area of somatic sensory innervations
Symptoms of dilated venules external hemorrhoid
Mildly symptomatic, pain after bowel movement, associated with poor hygiene, bleeding
Treatment of dilated venules external hemorrhoid
Dietary fibre, stool softeners, steroid cream (short course), pramoxine (Anusol), avoid prolonged straining
Symptoms of thrombosed external hemorrhoid
Very painful, more likely to bleed, resolve w/n 2wks, may leave perianal skin tag
Treatment of thrombosed external hemorrhoid
Treatment: thrombectomy: patient with acute thrombosis and present within 24 hours. After 24 hours is usually not effective – better managed by treating the pain with ice
Definition of anal fissure?
Tear of anal canal below dentate line (very sensitive squamous epithelium) usually due to constipation, 90% posterior midline, 10% anterior midline because the posterior midline is in the watershed area of blood supply; if off midline = consider other possible causes such as IBD/STI/TB/leukemia/anal carcinoma
Pathophysiology of anal fissure?
Repetitive Injury after 1st Tear: sphincter spasm occurs preventing edges from healing and leads to further tearing, ischemia may ensure and contribute to chronicity
Etiology of anal fissure?
- Local trauma: constipation, irritation, diarrhea, vaginal delivery, anal intercourse
- Secondary to: Crohn’s disease, granulomatous diseases, malignancy, communicable diseases
Signs and symptoms of acute anal fissure?
Acute: very painful BRBPR especially after bowel movement, sphincter spasm on limited DRE. Pain can last for hours after defecation Heals in 1-2 weeks with treatment
Signs and symptoms of chronic anal fissure?
Chronic: fissure, sentinel skin tags (Thickened mucosa/skin at the distal end of an anal fissure that is often confused with a small hemorrhoid), hypertrophied anal papillae; anal ulcer
Treatment of acute anal fissure?
Acute: conservative – stool softeners, bulking agents, sitz bath, analgesia
Treatment of chronic anal fissure?
- Conservative
- Topical Nitroglycerin or Nifedipine: ^local blood flow, promote healing/relieves sphincter spasm
- Botox: In the intersphincteric groove inhibits release of Ach, reducing sphincter spasm
- Lateral Internal Anal Sphincterotomy: (most effective, 90% heal successfully) cut the internal sphincter to release it from spasm, not often done, used in chronic fissure refractory to conservative treatment
Pathophysiology of anorectal abscess?
At the dentate line, there are crypts and anal glands. These glands extend through the internal sphincter into the intersphincteric space. When obstructed, this can lead to abscess in a number of potential spaces.
The most common spaces involved in anorectal abscesses are ____ and _____, totaling 80% of presentations.
Perianal
Ischiorectal
Causes of anorectal abscess?
Cryptoglandular abscess accounts for 90% of anorectal abscess/fistula disease. The remaining 10% are due to IBD, atypical infections such as TB or actinomycosis, trauma (both community acquired such as foreign body or impalement and hospital acquired such as episiotomy or prostatectomy), and malignancy
Common bacteria of anorectal abscess?
E. coli, proteus, streptococci, staphylococci, bacteriodes, anaerobes
Signs and symptoms of anorectal abscess?
Throbbing pain that may worsen with straining/ambulation, abscess can spread vertically downward (perianal), vertically upward (supralevator), or horizontally (ischiorectal), tender perianal/rectal mass on exam
Treatment of anorectal abscess?
Irrigation and debridement (curative in 50% of cases, 50% develop anorectal fistulas), may require antibiotics if DM/heart murmur/cellulitis, sitz bath, anal hygiene and stool softeners
Definition of anal fistula?
Fistula from anal canal to perianal skin; inflammatory tract w/ internal os at dentate line (almost always) + external os on anal skin. Most are cryptoglandular origin and go to the intersphincteric space.
Types of anal fistula?
- Intersphincteric 40%
- Trans-sphincteric 30% (through the external sphincter muscle).
- Suprasphincteric 20% very rare
- Extrasphincteric 10% - don’t start at the dentate line
Etiology of anal fistula?
Same processes that lead to the formation of an anal abscess, others (post op, trauma, anal fissure, malignancy, radiation proctitis). **THINK ABOUT CROHN’S
Signs and symptoms of anal fistula?
Intermittent or constant purulent d/c from perianal opening, pain, redness, tender, swelling, palpable cord-like tract, recurrent perirectal abscess
What is Goodall’s rule?
Fistulas originating anterior to a transverse line through the anus will have a straight course and exit anterior, whereas those originating posterior to the transverse line will begin in the midline and have a curved tract.
When does Goodall’s rule not apply?
Goodsall’s rule does not apply to patients with Crohn’s disease
Identification of anal fistula?
- Goodsall’s Rule
- Fibrous Tract: probing or fistulography under anesthesia
What is a simple anal fistula?
A simple anal fistula are low and include superficial, intersphincteric, or low transsphincteric fistulas. They also involve only one communicating tract and are not associated with inflammatory bowel disease (IBD) or other organs (bladder or vagina).
What is a complex anal fistula?
Complex fistulas are higher along the gastrointestinal (GI) tract, have multiple tracts, involve other organs, are recurrent, or are associated with IBD or radiation.
Are we more or less aggressive with cutting out the muscle when posterior anal canal is involved compared to the anterior anal canal.
Usually more aggressive cutting out muscle when posterior anal canal (especially in men), and less aggressive when anterior anal canal (especially in women)
What is a fistulotomy?
Fistulotomy: unroof tract from external to internal opening, allow drainage, heals by secondary intention (occurs when the sides of the wound are not opposed, therefore healing must occur from the bottom of the wound upwards)
Treatment of low lying fistula
Low lying fistula (does NOT involve external sphincter) > primary fistulotomy
Treatment of high lying fistula
High lying fistula (involves external sphincter) > staged fistulotomy with Seton suture placed through tract - Thick suture placed through fistula tract to allow slow transection of sphincter muscle; scar tissue formed will hold the sphincter muscle in place and allow for continence after transection (promotes drainage and fibrosis, decreases incidence of incontinence, delineates anatomy, usually done to spare muscle)
Treatment of complex anal fistula?
- For complex fistulas there is usually a primary track which is connected to the internal opening and secondary tracks arise from this. You want to control that primary track first with a seaton suture
- Tissue glue and fistula plug aim to fill the primary track with fibrosis and the external opening left open
- Ligation of Intersphincteric Fistula Tract (LIFT): alternative for high lying fistula – access fistula between sphincter muscles and ligate them, sparing them
Post-operative treatment of anal fistula?
Sitz bath, irrigation and packing to ensure healing from inside to outside (fistulas heal from the bottom up).
Definition of pilonidal disease
Cyst/abscess near or on the intergluteal cleft of the sacrococcygeal area containing hair/skin debris
Treatment of anal fistula
Surgery - Fistulotomy
Epidemiology of pilonidal disease
Epi: usually young men age 15-35yr, rare in >50
Pathophysiology of pilonidal disease
Obstruction of hair follicles > formation of cysts, sinuses, or abscesses, associated with occupations that require prolonged sitting, obesity, and high amounts of body hair. Friction and pressure — skin rubbing against skin, tight clothing, bicycling, long periods of sitting or similar factors — force the hair down into skin
Signs and symptoms of pilonidal disease
Asymptomatic or chronically itchy until acutely infected, then pain/tenderness, purulent discharge and increased moisture near the coccyx
Treatment of pilonidal disease
- Acute Abscess: irrigation and debridement, wound packed open, 40% develop chronic pilonidal sinuses
- Surgery: pilonidal cystotomy (excision of sinus tract and cyst, wound closed by secondary intention, primary closure with tissue flap or marsupialization
Signs and symptoms of proctalgia/levator ani syndrome
- Severe, episodic pain in the regions of the rectum and anus. It can be caused by cramping of the levator ani muscle, particularly in the pubococcygeal part
- It most often occurs in the middle of the night and lasts from seconds to minutes; pain and aching lasting twenty minutes or longer would likely be diagnosed instead as levator ani syndrome
- During an episode, the patient feels spasm-like, sometimes excruciating, pain in the rectum and/or anus, often misinterpreted as a need to defecate. To be diagnosed as proctalgia fugax, the pain must arise de novo (meaning the absence of clear cause).
Indications of pilonidal disease?
Failure of healing after irrigation/debride, recurrent disease, or complex disease
Most common tumor of anal canal
SSC of the anal canal
Clinical features of SSC of the anal canal
Anal bleeding, pain, mass, ulceration, pruritus, 25% asymptomatic
Treatment of SSC of the anal canal
Chemotherapy ± radiation ± surgery
3 types of anal cancer?
- SSC of the Anal Canal
- Malignant Melanoma of Anal Canal
- Anal Margin CA
Treatment of malignant melanoma of anal canal?
Wide excision or abdominal perineal resection ± chemoradiation
Who should get a pap test of the anus/risk factors for anal cancer?
Cigarette smokers, men who have sex with men, individuals with a history of immunosuppression (such as in HIV infection) and women with a history of cervical, vaginal and vulval cancer are at increased risk of getting anal cancer
Definition of chronic abdominal pain?
Pain that persists for more than 3 months either continuously or intermittently. Intermittent pain may be referred to as recurrent abdominal pain (RAP)
Etiology of chronic abdominal pain?
- Gastrointestinal Disorders
- Celiac Disease
- Chronic cholecystitis
- Chronic hepatitis - Upper abdominal discomfort, malaise, anorexia, Jaundice uncommon, In about one third of patients, a history of acute hepatitis
- Chronic pancreatitis - Episodes of severe epigastric pain, Sometimes malabsorption (eg, diarrhea, fatty stool), Usually a history of acute pancreatitis
- Colon cancer - Discomfort uncommon but possibly colicky discomfort if left colon is partially obstructed, Often occult or visible blood in stool
- Crohn Disease
- Gastric Cancer
- Inflammatory bowel disease
- Diverticular disease
- Irritable bowel syndrome
- Ulcer and non-ulcer dyspepsia (e.g., heartburn)
- Referred cardiothoracic pain - Genitourinary disease
- Endometriosis - Discomfort before or during menses GOOD
- Benign or malignant tumors - Vague lower abdominal discomfort, bloating. Sometimes a palpable pelvic mass
- Urinary tract disease
- Pelvic inflammatory disease
What should be asked on history for chronic abdominal pain?
- OPQRST
- Diet history - Milk products cause cramping/distension
- Concomitant GI symptoms such as gastroesophageal reflux, anorexia, bloating or “gas,” nausea, vomiting, jaundice, melena, hematuria, hematemesis, weight loss, and mucus or blood in the stool.
- Bowel symptoms, such as diarrhea, constipation, and changes in stool consistency, color, or elimination pattern
- PMHx
- Past surgical Hx
- Medications
Physical exam for chronic abdominal pain?
- Vitals
- General exam - jaundice, skin rash, and peripheral edema.
- Abdominal exam - areas of tenderness, presence of peritoneal findings (eg, guarding, rigidity, rebound), and any masses or organomegaly
Red flags of chronic abdominal pain?
Fever, Anorexia, weight loss, Pain that awakens patient, Blood in stool or urine, Jaundice, Edema, Abdominal mass or organomegaly
Investigations of chronic abdominal pain?
- Urinalysis, complete blood count, liver tests, blood urea nitrogen, glucose, and lipase
- Other tests: ultrasonography for ovarian cancer in women > 50 years, CT of the abdomen and pelvis with contrast, upper GI endoscopy (particularly in patients > 60 years old) or colonoscopy, and perhaps small-bowel imaging or stool testing.
Ddx for dyspepsia?
- NON GASTRIC CAUSES cardiac (myocardial infarction), pulmonary (pneumonia), hepatobiliary (biliary colic), pancreatic (pancreatitis), colonic (irritable bowel disease), musculoskeletal, dietary indiscretion
- PEPTIC ULCER DISEASE (PUD, 10 20%) H. pylori, ASA, NSAIDs (COX 2 inhibitors slightly decreased risk), cancer, Zollinger Ellison, smoking
- MEDICATION SIDE EFFECTS NSAIDs, ASA, theophylline, calcium channel blockers, erythromycin, metronidazole, bisphosphonates, orlistat, acarbose, iron, potassium supplements
- GASTROESOPHAGEAL REFLUX DISEASE (GERD, 20%)
- NON ULCER DYSPEPSIA (50%) cause unclear. Diagnosis of exclusion (rule out organic cause and irritable bowel disease)
Etiology of GERD?
- ACIDS*
- Acid hypersecretion Zollinger Ellison disease (gastrinomas, secrete large amounts of the hormone gastrin, which causes your stomach to produce too much acid)
- Alcohol abuse
- Connective tissue disease scleroderma
- Infections of esophagus CMV, HSV, candidiasis
- Diabetic gastroparesis
- Drug therapy
- Smoking
Definition of dyspepsia?
Chronic or recurrent epigastric pain, often with regurgitation, heartburn, bloating, nausea, and post prandial fullness (indigestion)
Definition of heartburn?
Retrosternal burning sensation secondary to lower esophageal sphincter relaxation = more specific for GERD
Approach to dyspepsia
- Consider non gastric causes of dyspepsia (cardiac, pulmonary, hepatobiliary, colonic, musculoskeletal, medications, and dietary indiscretion) and investigate those causes if likely. Otherwise proceed to step 2
- If age >50 or alarm symptoms Very BAD (Vomiting, Bleed/anemia, Abdominal mass/ weight loss, Dysphagia), refer for gastroscopy to check for gastric cancer. Otherwise proceed to step 3
- If ASA or NSAIDs use, stop medications if possible. If not, consider proton pump inhibitor/H2 blocker trial and proceed to step 4
- If GERD predominant symptoms (heartburn, regurgitation), treat as GERD. Otherwise, proceed to step 5
- If H. pylori urea breath test positive, treat with triple therapy. Otherwise, proceed to step 6
- If none of the above, diagnosis of non-ulcer dyspepsia
Investigations for dyspepsia
- Labs - CBCD, lytes, glucose, AST, ALT, ALP, bilirubin, lipase, Ca, albumin, fecal occult blood
- Imaging - upper GI series, U/S abd, CT abd
- Special tests – Urea beath test, H. Pyloria Serology, 24h Esophageal pH study, Endoscopy w/ biopsy and Culture, PPI inhibitor trial
Diagnosis of irritable bowel syndrome (IBS)?
Consider using Manning Criteria: 3 or more of the following with no red flags:
- Pain relief with bowel movement, more frequent stools with onset of pain, loose stools with onset of pain, passage of mucus, sensation of incomplete evacuation, abdominal distention
- Red Flags: Age >50 years, weight loss, blood in stools, anemia, fever
Symptoms of PUD
- Many patients with peptic ulcers remain asymptomatic, particularly older patients
- Common presentations of peptic ulcers are nonspecific, and symptoms are often intermittent/episodic due to spontaneous healing and relapse
- Gastric ulcer presentations include epigastric pain, often postprandial, dyspepsia, bloating and/or abdominal fullness, early satiety, nausea, vomiting, weight loss
Diagnosis of PUD?
- Peptic ulcer disease definitively diagnosed with endoscopy, but a Helicobacter pylori test-and-treat strategy (without endoscopy) may be used in some younger patients without alarm features
- Patients not receiving endoscopy, consider urea breath test (13C or 14C) or stool antigen tests (serologic antibody testing may also be used, but may have lower sensitivity and specificity than other noninvasive testing options)
Management of uncomplicated PUD?
Uncomplicated peptic ulcer in patients taking nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin: stop NSAID or aspirin use + PPI therapy (lansoprazole, omeprazole, pantoprazole for 4-6 weeks for duodenal ulcer, 6-8 weeks for gastric ulcer)
Management of H. pylori-positive PUD?
- Classic triple therapy CLAMET:
1. PPI (omeprazole) 20mg BID for 14 days
2. clarithromycin 500mg BID
3. Amoxicillin 1g BID and metronidazole
Presentation/symptoms of IBD?
Both present with chronic diarrhea, possibly bloody, abdo cramping, urgency.
Risk factors for IBD?
Age 15-40 y, jews, FHx of IBD, smoking (before for Crohn’s, after smoking cessation UC), western diet, NSAIDS
Features of Crohn’s
Distribution gum to bum, discrete skip lesions, usually rectal sparing, transmural disease, granulomas, Cobblestoning and creeping fat, strictures, and fistulas, more extraintestinal complications/Sx (arthritis, liver, blood, eyes/mouth, skin - erythema nodosum, kidney – calcium oxalate stones), perianal disease often
Complications of Crohn’s
Stricture, fistula, arthritis, irtis, episcleritis, erythema nodosum, pyoderma gangrenosum
Diagnosis of Crohn’s
- Colonoscopy + intubation of ileum*
- Biopsy & histology confirm diagnosis
- Gastroscopy to assess UGI
- Small Bowel Assessment – MR/CT enterography – thickened colonic wall, wireless capsule endoscopy
Symptoms of Crohn’s
Abdominal pain (esp. RLQ), diarrhea, Fe deficiency +/- anemia, fever, weight loss, growth failure, fatigue, pallor, malnutrition; gross bleeding uncommon, mucosal cobblestoning, gallstones, malabsorption, renal stones, hydronephrosis, amyloidosis
What does bx show for UC?
Biopsy shows inflamm confined to mucosa, distorted and branched crypts, abscesses crypts and plasma cells at base of crypt! Infectious colitis would have straight crypts
Symptoms of UC?
Usually chronic bloody diarrhea, abdominal cramping, urgency, tenesmus, incontinence, mild fever, tachycardia, dehydration, anemia
Diagnosis of UC?
- Lower endoscopy* (colitis begins in rectum + ascends)
- Always exclude infectious colitis → send stool for C + S, C.diff, O + P
- AXR leadpipe colon, thumbprinting CT – inflammation.
Complications of UC?
Toxic megacolon (colonic distension >6cm + fever, anemia, HR >120, neutrophils >10.5, dehydration, hypotension, altered sensorium, electrolyte disturbance), perforation, stricture, colon cancer
Features of UC?
Insidious onset, >4wks, chronic changes to mucosa→ mixed infiltrate, branched crypts, contiguous, mucosal disease, no granulomas.
Treatment of IBD?
Management of the 2 diseases are similar; however, in Colitis you can do a total colectomy to solve the problem. Surgery only used in Crohn’s to treat complications MED THERAPY IS THE MAINSTAY: start with mesalamine → antibio/probio → corticosteroids → immunosuppression → biologics (anti-TNF, anti-integrin therapy)→ surgery (mostly for UC).
95% of diverticular disease occurs in
Sigmoid colon
Risk factors of diverticulosis?
Lifestyle (low fiber diet [predispose to motility abnormalities and higher intraluminal pressure], in activity, obesity), muscle wall weakness from aging and illness (E.g. Ehler-Danlos, Marfan’s)
Symptoms and signs of diverticulosis?
Asymptomatic if uncomplicated (70-80%), painless massive bleeding, episodic abdo pain (often LLQ), bloating, flatulence, constipation, diarrhea, NO fever/leukocytosis, NO physical exam findings/poorly localized LLQ pain (most commonly in the sigmoid colon)
Treatment of diverticulosis?
- Uncomplicated: high fiber diet, education, mesalamine (5-ASA)
- Diverticular Bleed: initially work up and treat as any LGIB, if hemorrhage does not stop > resection
- Colonoscopy: Due to risk of perforation, this is performed 6 weeks after inflammation resolves to rule out colon cancer
Complications of diverticulosis?
Diverticulitis (15-25%), diverticulitis complicated with abscess/obstruction/perforation/fistula, bleeding (5-15% PAINLESS from rectum), diverticular colitis (rare: diarrhea, hematochezia, tenesmus, abdo pain)
Pathophysiology of diverticulosis?
High intraluminal pressures cause outpouching that occur at point of greatest weakness, most commonly where vasa recta penetrate the circular muscle layer, therefore increased risk of hemorrhage
Time period for acute viral hepatitis?
<6m
Time period for chronic viral hepatitis?
> 6m
Pathogenesis of viral hepatitis?
Virus infects hepatocytes creating MHC I proteins that are then attacked by CD8 T-cells for apoptosis leading to liver damage
Symptoms of viral hepatitis?
- Most are subclinical
- Flu-like prodrome may precede jaundice by 1-2wk
- Nausea/vomiting, anorexia, headaches, fatigue, myalgia, low-grade fever, arthralgia, and urticaria (especially HBV)
- Only some progress to icteric (clinical jaundice) phase, lasting days to weeks:
- pale stools and dark urine 1-5 d prior to icteric phase
- Hepatomegaly and RUQ pain
- Splenomegaly and cervical lymphadenopathy (10-20% of cases)
Investigations/findings for viral hepatitis?
- AST and ALT (> 10-20x normal in hepatocellular necrosis)
- ALP minimally elevated
- Viral serology:
- IgM antibody to HAV (IgM anti-HAV)
- Hepatitis B surface antigen (HBsAg)
- IgM antibody to hepatitis B core (IgM anti-HBc)
- Antibody to hepatitis C virus (anti-HCV) and hepatitis C RNA (HCV-RNA) PCR
- Increased urobilinogen (bile is broken down in UBG which is then transferred to the liver to convert back to bilirubin, but this isn’t happening
Treatment for viral hepatitis?
- Supportive (hydration, diet)
- Usually resolves spontaneously, but if severe HBV infection, treatment with entecavir should be considered; in anicteric hepatitis C, anti-viral treatment should be considered
- Indications for hospitalization: encephalopathy, coagulopathy, severe vomiting, hypoglycemia
Defective RNA virus requiring HBsAg for entry into hepatocyte, therefore infects only patients with HBV?
Hepatitis D
The presence of HBsAg indicates that the person is _____
Infectious
The presence of anti-HBs would be found in?
The presence of anti-HBs is generally interpreted as indicating recovery and immunity from hepatitis B virus infection. Anti-HBs also develops in a person who has been successfully vaccinated against hepatitis B.
In acute infection (<6 mos), anti-HBc is mainly of the ___ class, whereas in chronic infection, ___ anti-HBc predominates
IgM
IgG
Antibody to HBcAg (anti-HBc, or HBcAb would be found in?
Antibody to HBcAg (anti-HBc, or HBcAb) usually appears at the onset of clinical illness; thereafter, titers gradually diminish, usually over years or life. Its presence with anti-HBs indicates recovery from previous HBV infection. Anti-HBc is also present in chronic HBsAg carriers, who do not mount an anti-HBs response.
For hep B; ___ tends to suggest more active viral replication and greater infectivity. In contrast, presence of the corresponding antibody (____) suggests lower infectivity
HBeAg
anti-HBe
Standard of care for hep C treatment?
Oral interferon-free regimens
Mechanism by which acetaminophen induces damage on hepatocytes?
Mechanism: high acetaminophen dose saturates glucuronidation and sulfation elimination pathways - reactive metabolite is formed - covalently binds to hepatocyte membrane
Presentation of acetaminophen induced liver disease?
- First 24 h: nausea and vomiting (usually within 4-12 h of overdose)
- 24-48 h: asymptomatic, but ongoing hepatic necrosis resulting in increased transaminases
- > 48 h: continued hepatic necrosis possibly complicated with acute liver failure or resolution
Treatment of acetaminophen induced liver disease?
- gastric lavage/emesis (if <2 h after ingestion)
- oral activated charcoal
- N-acetylcysteine (NAC) can be given PO or IV (most effective within 8-10 h of ingestion, but should be given no matter when time of ingestion) - promotes hepatic glutathione regeneration
What is Wilson’s disease?
Copper builds up due to lack of ceruloplasmin (which normally binds it in liver). Affects other organs (esp brain). Mutation of copper transporting ATPase results in excess copper, autosomal recessive
Symptoms of Wilson’s disease?
- Asterixis
- Basal ganglia degeneration: suspect if parkinsonian features in the young Ceruloplasmin decreases
- Cirrhosis/hepatitis
- Corneal deposits (Kayser-Fleischer ring)
- Copper
- Dementia
- CNS: basal ganglia (wing flapping tremor, Parkinsonism), cerebellum (dysarthria, dysphagia, incoordination, ataxia), cerebrum (psychosis, affective disorder)
- Fanconi syndrome (malabsorption proximal tubule of kidney
- Blood: intravascular hemolysis; may be initial presentation in fulminant hepatitis
- Joints: arthritis, bone demineralization, calcifications
Screening test for Wilson’s disease?
- reduced serum ceruloplasmin (<50% of normal)
- Kayser-Fleischer rings (usually require slit-lamp examination)
- increased urinary copper excretion (measure 24-hour urine copper)
Gold standard for Wilson’s disease?
- increased copper on liver biopsy by quantitative assay
2. genetic analysis imperfect as many mutations in ATP7B are possible
Treatment for Wilson’s disease?
- penicillamine chelates copper, poorly tolerated
- trientine chelates copper
- zinc impairs copper excretion in stool and decreases copper absorption from gut
- tetrathiomolybdate preferred if neurological involvement
What is hemochromatosis?
Iron overload syndrome, autosomal recessive, common in Caucasians. Excessive iron storage causing multiorgan system dysfunction (liver, in particular) with total body stores of iron increased to 20-40 g (normal 1 g)
Etiology of primary (hereditary) hemochromatosis?
Hepcidin deficiency results in ongoing gut absorption of iron despite adequate iron stores
Etiology of secondary hemochromatosis
- Parenteral iron overload (e.g. transfusions)
- Chronic hemolytic anemia: thalassemia, pyruvate kinase deficiency
- Excessive iron intake
Clinical features of hemochromatosis
- Usually presents with trivial elevation in serum transaminases
- Liver: cirrhosis (less common nowadays due to earlier detection), HCC (200x increased risk)
- Pancreas: DM, chronic pancreatitis
- Skin: bronze or grey (due to melanin, not iron)
- Heart: dilated cardiomyopathy
- Pituitary: hypogonadotropic hypogonadism (impotence, decreased libido, amenorrhea)
- Joints: arthralgia (any joint, but especially MCP joints), chondrocalcinosis
Who should you screen and how to screen for hemochromatosis?
Screening for individuals with clinical features and/or family history (1/4 chance of sibling having the disease)
- Transferrin saturation (free Fe2+/TIBC) >45%
- Serum ferritin >400ng/mL
- HFE gene analysis: 90% of primary hemochromatosis involves C282Y allele, while H63D and S65C alleles also commonly involved and screened
Treatment of hemochromatosis?
- Phlebotomy: weekly or q2wk then lifelong maintenance phlebotomies q2-6mo
- Deferoxamine if phlebotomy contraindicated (e.g. cardiomyopathy, anemia)
- Primary hemochromatosis responds well to phlebotomy
- Secondary hemochromatosis usually requires chelation therapy (administration of agents that bind and sequester iron, and then excreted)
Most common cause chronic liver failure
Alcoholic liver disease
What are the three types of alcoholic liver disease
- Metabolic condition (fatty liver)
- Inflammatory condition (alcohol hepatitis)
- Fibrotic condition (cirrhosis)
Clinical features of fatty liver
Mildly tender hepatomegaly; jaundice rare, mildly increased transaminases <5x normal
Clinical features of mild alcohol hepatitis?
Mild: stops drinking because feels unwell, resumes when feeling better (if assessed, findings of hepatitis, potentially mild jaundice, and mildly elevated INR)
Clinical features of severe alcohol hepatitis?
Severe: stops drinking but feels unwell, low grade fever, RUQ discomfort, increased white blood cell count - mimics RLL pneumonia and cholecystitis
Investigations for alcoholic liver disease
- AST:ALT >2:1 (both usually <300)
- CBC: increased MCV, increased WBC often seen with alcoholic hepatitis but not necessarily in other alcohol-related liver injury
- Increased GGT
Treatment of alcoholic liver disease
- Alcohol cessation - Alcoholics Anonymous, disulfiram, naltrexone, acamprosate
- Multivitamin supplements (especially thiamine)
- Caution with drugs metabolized by the liver
- Prednisolone if severe alcoholic hepatitis based on Maddrey’s discriminant function or MELD score
Risk factors of non-alcoholic steatohepatitis (NASH)?
DM, Male, hyperlipidemia, obesity
Two types of non-alcoholic steatohepatitis (NASH)?
- Non-alcoholic fatty liver (NAFL): The term used when there is simple steatosis in the liver not accompanied by inflammation, cell injury or fibrosis. 25% of N. Americans
- NASH: The term used when steatosis is accompanied by inflammation and cell injury/ballooning degeneration with or without fibrosis (resembles alcoholic liver disease).
Presentation of non-alcoholic steatohepatitis (NASH)?
- Often asymptomatic
- May present with fatigue, malaise, and vague RUQ discomfort
- Elevated serum triglyceride/cholesterol levels and insulin resistance
Investigations of non-alcoholic steatohepatitis (NASH)?
- Elevated serum AST, ALT ± ALP; AST/ALT <1
- Presents as echogenic liver texture on ultrasound
Treatment of non-alcoholic steatohepatitis (NASH)?
- Mainstay is gradual weight loss (0.5-1kg/wk) as rapid weight loss can worsen liver disease. Ideally, aim to lose at least 7-10% of body weight
- Some evidence for vitamin E (800 U daily) if there is hepatic inflammation
- Some evidence for benefits of coffee drinking (3cups/d) and vitaminD
What is alpha-1-antitrypsin deficiency
A1AT inactivates elastase. Thus a deficiency results in elastase breaking down too much elastin. Thus, neutrophil elastase will go unchecked, breaking down elastin in the lungs. The acinus turns into one big cavity -this is emphysema. Can also lead to chronic bronchitis and COPD
Two types of alpha-1-antitrypsin deficiency
- Insufficient A1AT (unopposed elastase in lung – null or heterozygote allele WORST)
- Accumulation of A1AT (leading to cell dysfunction – ZZ allele is the WORST for this).
Presentation of alpha-1-antitrypsin deficiency
Early emphysema, neonatal hepatitis syndrome, or cirrhosis carcinoma, elevated liver enzymes
Diagnosis of alpha-1-antitrypsin deficiency
Serum A1AT level, Pi phenotype abnormal
Treatment of alpha-1-antitrypsin deficiency
NONE for liver type – just treat complications, screen for carcinoma. If lung type, then can give A1AT infusion! Screen family.
Definition of cirrhosis
Liver damage characterized by diffuse distortionofthebasicarchitecturewithfibrosisandformationof regenerative nodules
Etiology of cirrhosis
- Fatty liver (alcoholic or non-alcoholic fatty liver disease)
- Chronic viral hepatitis (B,B+D,C; not A or E)
- Autoimmune hepatitis
- Drugs (e.g. chronic methotrexate or amiodarone use)
- Hemochromatosis
- Primary biliary cholangitis
- Chronic hepatic congestion: cardiac cirrhosis (chronic right heart failure, constrictive pericarditis), hepatic vein thrombosis (Budd-Chiari)
Investigations of cirrhosis?
- Definitive diagnosis is histologic (liver biopsy)
- Blood work: fall in platelet count <150 is the earliest finding, followed many years later with rise in INR, fall in albumin, rise in bilirubin, fall in glucose level (pre-terminal event)
- Imaging
• U/S is the primary imaging modality but only finds advanced cirrhosis
• CT to look for varices, nodular liver texture, splenomegaly, ascites
• Transient Ultrasound Elastograhy: non-invasive tool using elastography (variable availability) for measuring liver compliance - Gastroscopy: varices or portal hypertensive gastropathy
Treatment of cirrhosis?
- Decrease insults (e.g. alcohol cessation, hepatotoxic drugs, immunize for Hep A and B if non-immune)
- Follow patient for complications (esophageal varices, ascites, HCC defines stage 2 cirrhosis)
- Liver transplantation for end-stage disease if no alcohol for >6mo; use MELD score
Hematologic changes in cirrhosis
- Pancytopenia from hypersplenism: platelets first, then WBC, then hemoglobin
- decreased clotting factors resulting in elevated INR
What is the strongest predictor of variceal development
Hepatic venous pressure gradient (HVPG) >10 mmHg
Treatment of variceal bleeds?
Resuscitation, antibiotic prophylaxis, vasoactive drugs (e.g. octreotide IV) combined with endoscopic band ligation or sclerotherapy, Transjugular Intrahepatic Portosystemic Shunt (TIPS)
Classification of renal failure in cirrhosis?
- pre-renal (usually due to over-diuresis)
- acute tubular necrosis
- Hepatorenal Syndrome (HRS)
What is type I hepatorenal syndrome (HRS)?
Type I: sudden and acute renal failure (rapid doubling of creatinine over 2 wk)
What is type II hepatorenal syndrome (HRS)?
Type II: gradual increase in creatinine with worsening liver function (creatinine doubling over years)
Hepatorenal syndrome (HRS) can occur at any time in severe liver disease, especially after:
- Overdiuresis or dehydration, such as diarrhea, vomiting, etc.
- GI bleed
- Sepsis
Treatment of hepatorenal syndrome?
- For type I HRS: octreotide + midodrine + albumin (increases renal blood flow by increasing systemic vascular resistance)
- Definitive treatment is liver transplant
Pathogenesis of hepatopulmonary syndrome?
Thought to arise from ventilation-perfusion mismatch, intrapulmonary shunting and limitation of oxygen diffusion, failure of damaged liver to clear circulating pulmonary vasodilators vs. production of a vasodilating substance by the liver
Clinical features of hepatopulmonary syndrome
- hyperdynamic circulation with cardiac output >7 L/min at rest and decreased pulmonary + systemic resistance (intrapulmonary shunting)
- dyspnea, platypnea (increase in dyspnea in upright position, improved by recumbency), and orthodeoxia (desaturation in the upright position, improved by recumbency)
Treatment of hepatopulmonary syndrome
Only proven treatment is liver transplantation
Diagnosis of hepatopulmonary syndrome
Diagnosis via contrast-enhanced echocardiography: inject air bubbles into peripheral vein; air bubbles appear in left ventricle after third heartbeat (normal = no air bubbles; in ventricular septal defect, air bubbles seen <3 heart beats)
Definition of portal hypertension
Pressure gradient between hepatic vein pressure and wedged hepatic vein pressure (corrected sinusoidal pressure) >5 mmHg
Pathophysiology of portal HTN?
- pre-sinusoidal (e.g. portal vein thrombosis, schistosomiasis, sarcoidosis)
- sinusoidal (e.g. cirrhosis, alcoholic hepatitis)
- post-sinusoidal (e.g. right-sided heart failure, hepatic vein thrombosis, veno-occlusive disease, constrictive pericarditis)
Signs of portal HTN?
Esophageal varices, Melena, Splenomegaly, Ascites, Hemorrhoids
Complications of portal HTN?
- GI bleeding from varices in esophagus, less commonly in stomach, even less frequently from portal hypertensive gastropathy
- ascites
- hepatic encephalopathy
- thrombocytopenia
- renal dysfunction
- sepsis
- arterial hypoxemia
Treatment of portal HTN?
- Non-selective B-blockers (propanolol, nadolol, carvedilol) decrease risk of bleeding from varices
- TIPS: to decrease portal venous pressure
Chronic stigmata of liver disease
Jaundice, asterixis, palmar erythema, dupuytren’s contracture(contraction of the tendons in the hand), leukonychia, ecchymosis, fetor hepaticus (a sign that your liver is having trouble doing its job of filtering out toxic substances), parotid hypertrophy, spider angiomas (often on neck or above), gynecomastia, caput medusae (appearance of distended and engorged superficial epigastric veins, which are seen radiating from the umbilicus across the abdomen), ascites, scleral icterus, umbilical hernia, esophageal varices, malnourished
Definition of hepatic encephalopathy?
Spectrum of potentially reversible neuropsychiatric syndromes secondary to liver disease diagnosed after ruling out other causes for symptoms (e.g. structural/metabolic)
Pathophysiology of hepatic encephalopathy?
Portosystemic shunt around hepatocytes and decreased hepatocellular function increase level of systemic toxins (believed to be ammonia from gut, mercaptans, fatty acids, amino acids) which go to the brain
Precipitating factors of hepatic encephalopathy?
- Nitrogen load (GI bleed, protein load from food intake, renal failure, constipation)
- Drugs (narcotics, CNS depressants)
- Electrolyte disturbance (hypokalemia, alkalosis, hypoxia, hypovolemia)
- Infection (spontaneous bacterial peritonitis)
- Deterioration in hepatic function or superimposed liver disease
Stages of hepatic encephalopathy?
I: apathy, restlessness, reversal of sleep-wake cycle, slowed intellect, impaired computational abilities, impaired handwriting
II: asterixis, lethargy, drowsiness, disorientation
III: stupor (rousable), hyperactive reflexes, extensor plantar response (upgoing Babinski)
IV: coma (response to painful stimuli only)
What needs to be ruled out in order to diagnosis hepatic encephalopathy?
- Non-liver-related neuropsychiatric disease in a patient with liver problems (e.g. alcohol withdrawal or intoxication, sedatives, subdural hematoma, metabolic encephalopathy)
- Causes of metabolic encephalopathy (e.g. renal failure, respiratory failure, severe hyponatremia, hypoglycemia)
Treatment of hepatic encephalopathy?
- Lactulose: titrated to achieve 2-3 soft stools/d
- Oral rifaximin for both acute treatment and maintenance therapy has high level evidence for efficacy
Why is lactulose used to treat hepatic encephalopathy?
- Prevents diffusion of NH3 (ammonia) from the colon into blood by lowering pH and forming non-diffusible NH4 (ammonium)
- Serves as a substrate for incorporation of ammonia by bacteria, promotes growth in bowel lumen of bacteria which produce minimal ammonia
- Also acts as a laxative to eliminate nitrogen-producing bacteria from colon
Definition of ascites?
Accumulation of excess fluid in the peritoneal cavity
What should be calculated in order to determine the etiology of ascites
Serum [Alb] – Ascitic [Alb]
Etiology of Serum [Alb] – Ascitic [Alb] >11 g/L (1.1 g/dL)
- Cirrhosis/severe hepatitis
- Chronic hepatic congestion
- Massive liver metastases
- Myxedema
Etiology of Serum [Alb] – Ascitic [Alb] <11 g/L (1.1 g/dL)
- Peritoneal carcinomatosis
- TB
- Pancreatic disease
- Serositis
- Nephrotic syndrome
Diagnosis of ascites
- Abdominal ultrasound
- Physical exam (clinically detectable when >500mL): bulging flanks, shifting dullness, fluid-wave test positive. Most sensitive symptom: ankle swelling
Treatment of diuretic-sensitive ascites
- Na+ restriction (daily sodium intake <2 g)
- diuretics: spironolactone, furosemide
- aim for weight loss 0.5-1 kg/d, more if concomitant peripheral edema (which is mobilized quicker than ascitic fluid); overly rapid weight loss increases risk of renal failure
- if target weight loss is not achieved and there are no complications, increase dose to achieve target while monitoring for complications
Treatment of refractory ascites
- Therapeutic paracentesis with intravenous albumin
- TIPS in anappropriate patient (no contraindications) with potential ltransplant-free survival advantage
- Liver transplantation
Who should be on prophylaxis for spontaneous bacterial peritonitis (SBP)
- Cirrhosis or GI bleed: ceftriaxone IV daily or norfloxacin bid x7d
- Previous episode of SBP: long-term prophylaxis with daily norfloxacin or TMP-SMX
Clinical features of spontaneous bacterial peritonitis (SBP)
- 1/3 of patients are asymptomatic, thus do not hesitate to do a diagnostic paracentesis in ascites even if no clinical indication of infection
- Fever, chills, abdominal pain, ileus, hypotension, worsening encephalopathy, acute kidney injury
Diagnosis of spontaneous bacterial peritonitis (SBP)
- Culture, count and Albumin (also get serum albumin content)
- Absolute neutrophil count in peritoneal fluid >0.25 x109 cells/L (250 cells/mm3)
- Gram stain positive in only 10-50% of patients
Treatment of spontaneous bacterial peritonitis (SBP)
- IV antibiotics (cefotaxime 2g IV q8h or ceftriaxone 2g IV daily is the treatment of choice for 5d; modify if response inadequate or culture shows resistant organisms)
- IV albumin (1.5g/kg at time of diagnosis and 1g/kg on day 3) decreases mortality by lowering risk of acute renal failure
Etiology of vomiting and/or nausea?
- Infectious – Gastroenteritis (viral and bacterial)
- Gastrointestinal system
- Drugs - chemotherapeutic agents, opioids, cannabis
- CNS
- Endocrinologic and metabolic: Pregnancy, Other endocrine and metabolic – Uremia, Diabetic ketoacidosis, Hyperparathyroidism, Hypoparathyroidism, Hyperthyroidism, Addison’s disease, Acute intermittent porphyria
- Others: Postoperative nausea and vomiting, Cyclic vomiting syndrome, Cardiac disease - Myocardial infarction, Heart failure, Starvation, Radiation therapy to the upper abdomen and lower chest
Causes of gastrointestinal system vomiting and/or nausea?
- Mechanical obstruction - Gastric outlet obstruction, Small bowel obstruction
- Functional gastrointestinal disorders
- Gastroparesis
- Chronic intestinal pseudo-obstruction
- Nonulcer dyspepsia
- Irritable bowel syndrome
- Organic gastrointestinal disorders - Pancreatic adenocarcinoma, Inflammatory intraperitoneal disease, Peptic ulcer disease, Cholecystitis, Pancreatitis, Hepatitis, Crohn disease, Mesenteric ischemia, Retroperitoneal fibrosis, Mucosal metastases
Causes of CNS vomiting and/or nausea?
- Migraine
- Increased intracranial pressure – Malignancy, Hemorrhage, Infarction, Abscess, Meningitis, Congenital malformation, Hydrocephalus, Pseudotumor cerebri
- Seizure disorders
- Emotional responses
- Psychiatric disease - Psychogenic vomiting, Anxiety disorders, Depression, Pain, Anorexia nervosa, Bulimia nervosa
- Labyrinthine disorders – Labyrinthitis, Ménière’s disease, Motion sickness
What should be asked on history for vomiting and/or nausea?
- Onset of symptoms – abrupt or insidious
- Timing of symptoms
- Nature of matter
- Abdominal pain
- Associated symptoms/findings
What could timing of symptoms tell you about vomiting and/or nausea?
- Before breakfast - Ethyl alcohol, increased intracranial pressure, pregnancy, uremia
- During or directly after eating - Psychiatric causes
- One to four hours after a meal - Gastric outlet obstructions (e.g., from peptic ulcer disease, neoplasms), gastroparesis
- Continuous - Conversion disorder, depression
What could nature of matter tell you about vomiting and/or nausea?
- Undigested food - Achalasia, esophageal disorders (e.g., diverticulum, strictures)
- Partially digested food - Gastric outlet obstruction, gastroparesis
- Bile - Proximal small bowel obstruction
- Feculent or odorous - Fistula, obstruction with bacterial degradation of contents
- Large volume (> 1,500 mL per 24 hours) - Suggests organic rather than psychiatric causes
What could abdominal pain tell you about vomiting and/or nausea?
- Right upper quadrant - Biliary tract disease, cholecystitis
- Epigastric - Pancreatic disease, peptic ulcer disease
- Severe pain - Biliary disease, pancreatic disease, peritoneal irritation, small bowel obstruction
- Severe pain that precedes vomiting
- Small bowel obstruction
What could associated symptoms/findings tell you about vomiting and/or nausea?
- Weight loss - Malignancy (significant weight loss may also occur secondary to sitophobia in gastric outlet obstructions and peptic ulcer disease)
- Diarrhea, myalgias, malaise, headache, contact with ill persons - Viral etiologies
- Headache, stiff neck, vertigo, focal neurologic deficits - Central neurologic causes (e.g., encephalitis/meningitis, head injury, mass lesion or other cause of increased intracranial pressure, migraine)
- Early satiety, postprandial bloating, abdominal discomfort - Gastroparesis
- Repetitive migraine headaches or symptoms of irritable bowel syndrome – cyclic vomiting syndrome
Physical exam of vomiting and/or nausea?
- Signs of dehydration
- General: jaundice, lymphadenopathy, and signs of thyrotoxicosis
- Signs of bulimia: dental enamel erosion, parotid gland enlargement, lanugo-like hair, and calluses on the dorsal surface of the hand
- Abdo exam: tenderness, distension, hernias
- Neuro
Investigations of vomiting and/or nausea?
- CBC, lytes, CRP, Cr, Ca, glucose
- bHCG, lipase, liver enzymes, protein/albumin, TSH
- Abdo Xray, possible CT
- Endoscopy
- Small bowel follow-through
- Enteroclysis
- Gastric motility studies (e.g., gastric emptying scintigraphy, cutaneous electrogastrography, antroduodenal manometry) may be considered.
What are the dopamine receptor blockers for the treatment of vomiting and/or nausea?
Dopamine receptor blockers are metoclopramide and haloperidol. Hits GI/CRTZ causes. Useful for chemical causes (meds). Don’t give these two together because it can induce extrapyramidal symptoms (EPS)
What are the prokinetic agents for the treatment of vomiting and/or nausea?
- Prokinetic agents (to remove constip) are metoclopramide and domperidone (Motilium). For stasis and ileus. Motilium doesn’t work on the brain, only on the gut but also can cause cardiac abnormalities. Maxeran can rarely cause extrapyramidal symptoms and delirium
- Agents with mainly prokinetic properties include erythromycin (motilin receptor agonist) and bethanechol (muscarinic receptor agonist).
1st line treatment for the treatment of vomiting and/or nausea?
Prochlorperazine is an antiemetic that often partially alleviates acute nausea and vomiting (eg, acute gastroenteritis), but is associated with risks of hypotension and extrapyramidal side effects
What are the serotonin receptor blockers for the treatment of vomiting and/or nausea?
Serotonin receptor blockers are Ondansetron (Zofran) and granisetron. Target 5HT receptors in CRTZ and vomiting centers. Doesn’t impact dopamine receptors so good when risk of EPS is high. They’ve become standard in chemo pre-treatment. No impact on motion sickness.
Signs and symptoms of jaundice?
- Dark urine, pale stools: suggests that bilirubin elevation is from direct fraction
- Pruritus: suggests chronic disease, cholestasis
- Abdominal pain: suggests biliary tract obstruction from stone or pancreatic tumour (obstructive jaundice)
- Painless jaundice in the elderly: think of pancreatic cancer, although most patients with pancreatic cancer have pain
- Kernicterus: rarely seen in adults due to maturation of blood brain barrier
Etiology of unconjugated hyperbilirubinemia (pre-hepatic)?
- Overproduction (hemolysis, reabsorption of hematoma)
- Decreased hepatic uptake (congestive heart failure)
- Decreased bilirubin conjugation (Gilbert syndrome, neonatal jaundice)
Investigations of jaundice?
- Blood work: CBC, bilirubin (direct and total), liver enzymes (AST, ALT, ALP, GGT), liver function tests (INR/PT, PTT, albumin), amylase
- Hepatitis viral and autoimmune serologic tests, blood smear
- U/S or CT for evidence of bile duct obstruction (e.g. bile duct dilation)
- MRCP: non-invasive
- EUS: sensitive for stones and pancreatic tumours
- ERCP: invasive,most accurate,allows for therapeutic intervention
- Percutaneous transhepatic cholangiography (PTC): if ERCP fails (endoscopic access not possible)
Etiology of conjugated hyperbilirubinemia (hepatic)?
- Intrahepatic cholestasis
- Common: Alcohol-related liver disease, drugs, toxins, viral hepatitis
- Less common: Infiltrative disorders (eg, amyloidosis, lymphoma, sarcoidosis, tuberculosis), pregnancy, primary biliary cholangitis, steatohepatitis - Extrahepatic cholestasis
- Common: Common bile duct stone, pancreatic cancer
- Less common: Acute cholangitis, pancreatic pseudocyst, primary sclerosing cholangitis, common duct strictures caused by previous surgery, other tumors - Hepatocellular injury
- Common: Drugs, toxins, viral hepatitis
- Less common: Alcohol-related liver disease, hemochromatosis, primary biliary cholangitis, primary sclerosing cholangitis, steatohepatitis, Wilson disease - Other (e.g., infiltrative states, fatty liver)
Definition of primary biliary cholangitis (PBC)
Chronic inflammation and fibrous obliteration of intrahepatic bile ductules
Etiology of primary biliary cholangitis (PBC)
Likely autoimmune (associated with Sjogren’s syndrome, scleroderma, CREST syndrome, rheumatoid arthritis (RA), thyroiditis)
Epidemiology of primary biliary cholangitis (PBC)
Affects mainly middle-aged women (M:F=1:9)
Signs and symptoms of primary biliary cholangitis (PBC)
- Often asymptomatic
- Initial symptoms: pruritus, fatigue
- Chronic: jaundice and melanosis (darkening skin) and other signs of cholestasis
- End-stage: hepatocellular failure, portal HTN, ascites
- High incidence of osteoporosis
Investigations of primary biliary cholangitis (PBC)
- Increased ALP, GGT; bilirubin rises in later stage
- Positive anti-mitochondrial antibodies (AMA; 95% specificity and sensitivity)
- elevated IgM
- increased serum cholesterol (mild increase in LDL, larger increase in HDL). may have: xanthelasmas, xanthomas
- liver biopsy confirms diagnosis and stages severity → mononuclear infiltrate centered on bile ducts + granulomas
- Normal bile duct on MRCP rules out bile duct obstruction which can mimic PBC
Treatment of primary biliary cholangitis (PBC)
- ursodiol (usual first line treatment)
- obeticholic acid (particularly if inadequate response to urosiol)
- cholestyramine (for pruritus and hypercholesterolemia)
- Calcium and vitamin D for low bone density; bisphosphonates if osteoporosis severe
- Monitor for thyroid disease
- Liver transplant if disease severe
Definition of ascending cholangitis
Infection of the biliary tree
Etiology of ascending cholangitis
- Stasis in the biliary tract due to obstruction or stricture (usually from previous cholecystectomy)
- Infection originates in the duodenum or spreads hematogenously from the portal vein
Signs and symptoms of ascending cholangitis
- Charcot’s triad: fever, RUQ pain, jaundice (50-70%)
- Reynolds’ pentad in patients with suppurative cholangitis: fever, RUQ pain, jaundice, hypotension, altered mental status
Investigations of ascending cholangitis
- Increased WBC
- Usually increased ALP and bilirubin, ALT variably elevated
- Blood culture
- Abdominal U/S: CBD dilation, stones
Treatment of ascending cholangitis
- Most important is drainage, ideally via ERCP; perform by percutaneous biliary or by surgical routes (least often) if ERCP not possible
- Antibiotic therapy: broad spectrum to cover Gram-negatives, Enterococcus, and anaerobes (especially if CBD manipulation)
Definition of primary sclerosing cholangitis (PSC)
Chronic inflammation + fibrosis of bile ducts in response to portal bacteria in genetically predisposed, progresses to liver failure over 12 years
What is idiopathic primary sclerosing cholangitis (PSC) often associated with?
Primary/idiopathic (most common) - associated with IBD, more commonly UC, in up to 70-80% of patients (usually male) with PSC
Secondary causes of primary sclerosing cholangitis (PSC)
- long-termcholedocholithiasis
- cholangiocarcinoma
- surgical/traumatic injury (iatrogenic)
- contiguous inflammatory process
- post-ERCP
- associated with HIV/AIDS (“HIV cholangiopathy”)
- IgG4-related disease
Signs and symptoms of primary sclerosing cholangitis (PSC)
- Often insidious, may present with fatigue and pruritus
- May present with signs of episodic bacterial cholangitis secondary to biliary obstruction
Investigations of primary sclerosing cholangitis (PSC)
- Increased ALP (hallmark), less often increased bilirubin
- Mildly increased AST, usually <300U/L
- p-ANCA (30-80%), elevated IgM (40-50%)
- MRCP and ERCP shows narrowing and dilatations of bile ducts that may result in “beading”, both intrahepatic and extrahepatic bile ducts
- if intrahepatic narrowing only, do anti-mitochondrial antibody to rule out PBC
Treatment of primary sclerosing cholangitis (PSC)
- Image bile duct (MRCP) at least annually for early detection of cholangiocarcinoma
- Endoscopic sphincterotomy, biliary stent in selected cases of dominant common bile duct stricture
- Antibiotics for cholangitis
- Suppurative cholangitis requires emergency drainage of pus in common bile duct
- Liver transplant
What is Gilbert’s syndrome?
- Metabolic defect- failure of bilirubin conjugation (UDP transferase). Normal Hb, Normal liver enzymes. Benign, non-progressive, COMMON
- Isolated unconjugated hyperbilirubinemia
Males or females more likely to get abdominal hernia?
M:F=9:1
Risk factors for abdominal hernia?
- Obesity, chronic cough, asthma, COPD, pregnancy, constipation, bladder outlet obstruction, ascites, and heavy lifting
- Congenital abnormality (e.g. patent processus vaginalis, and indirect inguinal hernia)
- Previous hernia repair, especially if complicated by wound infection
- Loss of tissue strength and elasticity (e.g. hiatus hernia, aging, and repetitive stress)
Clinical features of abdominal hernia?
- Mass of variable size
Tenderness worse at end of day, relieved with supine position or with reduction
Abdominal fullness, vomiting, constipation - Transmits palpable impulse with coughing or straining
Investigations for abdominal hernia?
- Physical examination usually sufficient
- U/S ¬ ± CT (CT required for obturator hernias, internal abdominal hernias, and Spigelian and/or femoral hernias in obese patients)
What is defined as a reducible hernia?
When the contents can be replaced through the hernia defect. Repair is either deferred or done electively
What is defined as a strangulated hernia?
Vascular supply of protruded viscus is compromised (ischemia). Requires emergency repair
What is defined as an incarcerated hernia?
Incarcerated hernia contents are unable to be replaced through the defect. Is indication for emergency surgery if contains small bowel, are otherwise repaired electively, Not necessarily strangulated
Why do epigastric hernias develop?
Develop due to developmental deficiencies, congenital umbilical hernia, or may occur due to weakness in the linea alba in the area of the umbilicus (acquired umbilical hernia)
Who are more likely to develop epigastric hernias
10x more common in women, also common in children but usually closes by age 2 – ideally fix them at age 5 if not (fewer than 5% persist into later childhood/adulthood)
What causes an incisional hernia?
Results from poor wound healing in a previous surgical incision (infection, tension, malnutrition, intra-abdominal pressure, etc.) – occurs in 5-10% of abdo incisions
What is a Littre’s hernia?
Hernia involving a Meckel’s diverticulum (Think alphabetically: Littre’s Meckel’s = LM)
What is an spigelian hernia?
Hernia through the linea semilunaris (or spigelian fascia); also known as spontaneous lateral ventral hernia (Think: Spigelian = Semilunaris)
What is a pantaloon hernia?
Hernia sac exists as both a direct and indirect hernia straddling the inferior epigastric vessels and protruding through the floor of the canal as well as the internal ring (two sacs separated by the inferior epigastric vessels [the pant crotch] like a pair of pantaloon pants)
What is a Richter’s hernia?
Only part of bowel circumference (usually anti-mesenteric border) is incarcerated or strangulated so may not be obstructed
What is a sliding hernia?
Part of wall of hernia sac formed by retroperitoneal structure (usually colon)
What is diastasis of the rectus abdominis muscles (DRAM)?
Diastasis of the rectus abdominis muscles (DRAM) is characterised by thinning and widening of the linea alba
Which types of hernias are more likely to strangulate?
Femoral»_space; indirect inguinal > direct inguinal
What are the indications for laparoscopic inguinal hernia repair?
- Bilateral inguinal hernias
- Recurring hernia
- Need to resume full activity as soon as possible
Treatment of abdominal hernia?
- Surgical treatment (herniorrhaphy) is only to prevent strangulation and evisceration, for symptomatic relief, for cosmesis; if asymptomatic can delay surgery
- Observation is acceptable for small asymptomatic inguinal hernias
Surgical technique for herniorrhaphy?
- Repair may be done open or laparoscopic and may use mesh for tension-free closure
- Avoid mesh for emergent cases with bowel compromise given risk of infection
- Most repairs are now done using tension free techniques (Lichtenstein) -a plug in the hernial defect and a patch over it or patch alone
Components of the spermatic cord
Vas deferens, Testicular artery, Artery of the ductus deferens, Cremasteric artery, Pampiniform plexus, Genital branch of the genitofemoral nerve (sensation to lateral scrotum), Parasympathetic and sympathetic nerves. Remember the ilioinguinal nerve runs outside of the spermatic cord The gubernaculum attaches the testicle to the scrotum
Boundaries of Hesselbach’s triangle?
Inferior epigastric vessels, Inguinal ligament (Poupart’s), Lateral border of the rectus sheath. Floor consists of internal oblique and the transversus abdominis muscle
Etiology of direct inguinal
Acquired weakness of transversalis fascia “Wear and tear”. Increased intra-abdominal pressure
Anatomy of direct inguinal
Through Hesselbach’s triangle Medial to inferior epigastric artery Usually does not descend into scrotal sac
Etiology of indirect inguinal
Congenital persistence of processus vaginalis in 20% of adults
Most common hernia in men and women
Indirect inguinal
Symptoms of indirect inguinal
Generally symptoms include an intermittent bulge in the inguinal region to vague pain or discomfort and occasionally paresthesia (compression of inguinal nerves – ilioinguinal nerve (pain in groin) and/or genital branch of the genitofemoral nerve). Ask about pain/bulge at night (there shouldn’t be any pain at night)
Treatment of indirect inguinal
- All babies with inguinal hernias need repair ASAP
- All with incarcerated or strangulated hernia need repair urgently, have higher rates of strangulation compared to direct hernias
- Elective herniorrhaphy is indicated to prevent the chance of incarceration/strangulation
Anatomy of indirect inguinal
Originates in deep inguinal ring Lateral to inferior epigastric artery Often descends into scrotal sac (or labia majora)
Epidemiology femoral hernia?
Affects mostly females
Etiology of femoral hernia?
Pregnancy – weakness of pelvic floor musculature. Increased intra-abdominal pressure
Anatomy of femoral hernia?
- Into femoral canal, below inguinal ligament but may override it. Medial to femoral vein within femoral canal
- Femoral Canal: femoral nerve > artery > vein > empty space (CANAL) > lymph nodes/lacunar ligament
Treatment of femoral hernia?
SHOULD ALWAYS BE REPAIRED - McVay (Cooper’s ligament repair), mesh plug repair
Two mechanisms of abdominal injuries
- Blunt: usually causes solid organ injury
- Penetrating: usually causes hollow organ injury or liver injury (most common)
What are the views of FAST scan?
CARDIAC VIEW + LUQ VIEW + RUQ VIEW + PELVIC VIEW + ANTERIOR LUNG FIELD
Most common organs to be injured in blunt trauma?
SPLEEN* > LIVER > MESENTARY > UROLOGIC > PANCREAS
Two types of hemorrhage for blunt trauma?
Intra-abdominal and retroperitoneal
Physical exam for blunt trauma
- Abdomen
- inspect: contusions, abrasions, seat-belt sign, distention
- auscultate: bruits, bowel sounds
- palpate: tenderness, rebound tenderness, rigidity, guarding
- DRE: rectal tone, blood, bone fragments, prostate location
- placement of NG, Foley catheter should be considered part of the abdominal exam - Other systems to assess: cardiovascular, respiratory (possibility of diaphragm rupture), genitourinary, pelvis, back/neurological
Investigations for blunt trauma
Labs: CBC, electrolytes, coagulation, cross and type, glucose, Cr, CK, lipase, amylase, liver enzymes, ABG, blood EtOH, B-hCG, U/A, toxicology screen
Imaging is done for blunt trauma if?
- Equivocal abdominal examination, altered sensorium, or distracting injuries (e.g. head trauma, spinal cord injury resulting in abdominal anesthesia)
- unexplained shock/hypotension
- patients have multiple traumas and must undergo general anesthesia for orthopedic, neurosurgical, or other injuries
- fractures of lower ribs, pelvis, spine
- positive FAST
Management of blunt trauma?
- General: ABCs, fluid resuscitation, and stabilization
- Surgical: watchful waiting vs. laparotomy
- Solid organ injuries: decision based on hemodynamic stability, not the specific injuries
- Hemodynamically unstable or persistently high transfusion requirements: laparotomy
- Hollow organ injuries: laparotomy
List the indications for a trauma laparotomy
- Hemodynamically unstable from abdominal trauma
- Peritonitis
- Evisceration
- Free air
- Certain injuries (confirmed or suspicious): Hollow viscious injuries, Diaphragmatic injury, Intraperitoneal bladder injury, ureteric injury, Pancreatic injury, Transaxial GSW
- Failure of nonoperative management
Indications for foley and NG tube in abdominal trauma?
Foley catheter: unconscious or patient with multiple injuries who cannot void spontaneously or is unconscious
Indications for NG tube in abdominal trauma?
NG tube: used to decompress the stomach and proximal small bowel. Contraindicated if suspected facial or basal skull fractures
Most common organs injured in penetrating trauma?
SMALL BOWEL > LIVER > COLON > STOMACH > DIAPHGRAM
Management of penetrating trauma?
- General: ABCs, fluid resuscitation, and stabilization
- Gunshot wounds always require laparotomy
Etiology of acute abdominal pain?
- GI Disorders
- Hepatobiliary
- Genital
- Urinary: Pyelonephritis, Renal colic, cystitis
- CVS: MI, aortic dissection, AAA, Pericarditis
- Resp: PE, empyema, pneumonia
- Metabolic: DKA, sickle cell crisis, toxin, Addisonian crisis, Lead poisoning, porphyria
- Other: Abdominal wall injury, herpes zoster, psychiatric, abscess, hernia, mesenteric adenitis
GI disorder aetiologies for acute abdominal pain?
- Perforated viscus, bowel obstruction, ischemic bowel, appendicitis, strangulated hernia, IBD flare, esophageal rupture, peptic ulcer disease
- Diverticulitis, gastroenteritis, GERD, esophagitis, gastritis, IBS
Hepatobiliary aetiologies for acute abdominal pain?
- Hepatic/splenic injury, pancreatitis, cholangitis, spontaneous bacterial peritonitis, Biliary colic, cholecystitis, hepatitis
Genital aetiologies for acute abdominal pain?
Female: Ovarian torsion, PID, ectopic pregnancy, tubo-ovarian abscess, ovarian cyst, salpingitis, endometriosis
Male: Testicular torsion, epididymitis, prostatitis
Red flags of acute abdominal pain?
Severe pain + signs of shock + peritoneal signs + abdominal distention + pain out of proportion to clinical findings + new onset pain/change in pain/altered bowel habits in elderly + weight loss + BRBPR/melena + anemia + supraclavicular nodes + FHx of serious bowel disease
Imaging for acute abdominal pain?
- AXR: look for calcifications, free air, gas pattern, air fluid levels
- CXR upright: look for pneumoperitoneum (free air under diaphragm), lung disease
- U/S: biliary tract, ectopic pregnancy, AAA, free fluid
- CT: trauma, AAA, pancreatitis, nephro-/urolithiasis, appendicitis, and diverticulitis
Labs for acute abdominal pain?
CBC, electrolytes, glucose, BUN/Cr, U/A ± liver enzymes, LFTs, amylase + lipase, B-hCG, ECG, troponins, VBG/lactate , INR/PTT, tox screen
Classic triad of AAA?
- acute abdominal or back pain 2. hypotension 3. pulsatile abdominal mass
Indications for surgery repair of AAA?
Indications for surgery >6cm diameter, painful/tender on palpation, enlarging, distal emboli, thrombosis, obstruction/compression of adjacent viscera, rupture
Diagnosis of AAA?
- Often incidental
- Confirmation by ultrasonography or abdominal CT
- Sometimes CT angiography or magnetic resonance angiography
- Most abdominal aortic aneurysms are diagnosed incidentally when they are detected during physical examination or when abdominal ultrasonography, CT, or MRI is done for other reasons. An AAA should be considered in older patients who present with acute abdominal or back pain whether a palpable pulsatile mass is present or not.
Treatment of AAA?
Control of atherosclerotic risk factors, especially smoking cessation and use of antihypertensive drugs as appropriate, is important. If a small or moderate-sized aneurysm becomes > 5.0 to 5.5 cm and if risk of perioperative complications is lower than estimated risk of rupture, AAA repair is indicated. Risk of rupture vs that of perioperative complications should be discussed frankly with the patient.
What is ectopic pregnancy?
Any pregnancy that is implanted outside of the endometrial lining in the uterine cavity. Most happen in the fallopian tubes
Risk factors of ectopic pregnancy?
- Prior ectopic pregnancy
- PID – usually chlamydia or gonorrhea (recurrence rate if PID flare - 1 prior flare (13%), 2 (35%), 3 (75%))
- Tubal surgery, tubal ligation failure
- Smoking
- IUD failure (decreases pregnancy rate, but if fails then 50% likelihood)!
- Infertility/IVF
- Age <18 or >35
Presentation of ectopic pregnancy?
Classic triad of amenorrhea, bleeding, and abdominal pain usually at 6-8wks.
Signs and symptoms of pancreatitis?
Abdominal pain/tenderness acute onset and then constant(epigastric, band-link, radiates to the back, sharp, worse when supine) + postprandial pain, constant N/V + guarding upper abdo + fever + tachycardia (SIRS or infection), orthostatic hypotension
Common causes of pancreatitis?
- Idiopathic
- Gallstones (or other obstructive lesions)
- EtOH
- Trauma
- Steroids
- Mumps (& Other Viruses – CMV, EBV)
- Autoimmune (SLE, polyarteritis nodosa)
- Scorpion sting
- Hyper Ca2+, High Triglycerides
- ERCP (5-10% of patients undergoing the procedure)
- Drugs (thiazides, sulfonamides, ACE-I, NSAIDS, azathioprine)
Labs for pancreatitis?
CBC + Lytes + Urea + Creatinine + ALT/ALP + Total/Direct Bilirubin + Lipase (specific) + amylase
Imaging for pancreatitis?
Abdo RUQ U/S (used to r/o cholelithiasis and to assess for choledocholithiasis) + CT Scan (key study) – comment of extent of inflammation, presence of fluid collection and extent of necrosis + AXR - Sentinel loop, colon cutoff, possibly gallstones (only 10% visible on x-ray)
Complications of pancreatitis?
WORSENING OF CO-MORBIDITIES. Fluid sequestration, dehydration, acute sequelae (peripancreatic fluid collection, phlegmon, pancreatic necrosis (infection), SIRS), chronic sequelae including pseudocyst (sterile/infected), obstruction (gastric/duodenal/biliary), pseudoaneurysms (splenic/gastric/hepatic/aortic), Hemosuccus Pancreaticus (erosion of pseudoaneurysm into PD causing an UGB), erosion/perforation (colon/duodenum), pancreatic ascites, pancreatic fistula, pleural effusions, splenic/portal/SMV thrombosis, diabetes
What is a pseudocyst?
Fluid-filled cyst in the lesser sac filled with digestive enzymes (amylase/lipase) – no epithelial lining, formed of inflammatory fibrosis; these are under high pressure and can erode into vital structures, they can become infected, and can get massive, blocking outflow of the stomach or crush/occlude the splenic or portal vein. 50% resolve spontaneously
Treatment options for pseudocyst?
Percutaneous aspiration/drain, Operative drainage, Transpapillary stent via ERCP (pseudocyst must communicate with pancreatic duct). If infected – add IV antibiotics. Must bx the cyst wall to rule out a cystic carcinoma (e.g., cystadenocarcinoma)
Treatment of gallstone pancreatitis?
Cholecystectomy after inflammation has resolved but before discharge
Management of pancreatitis?
- Determine Etiology: hx of EtOH/gallstones (most common)/trauma/drugs, U/S to look for cholelithiasis, and workup (^Ca/TG?)
- Resuscitation + Supportive Care: IV fluids/foley + early feeding (within 24-48 hrs, if can’t tolerate oral try NGT or NJT) + pain management (not morphine), correction of coags/electrolytes
- Adjuncts: CT Scan to look for complications (abscess, necrosis, sterile acute fluid collections, pseudocyst, infection, bleeding or ERCP for persistent non-resolving biliary obstruction in gallstone pancreatitis
- Surgery
Treatment of necrotizing pancreatitis?
Step up approach of Percutaneous drain -> endoscopic transgastric drainage -> minimally invasive retroperitoneal necrosectomy
Treatment of pancreas abscess?
Antibiotics and percutaneous drain placement or operative debridement and placement of drains
Most common etiology of acute appendicitis in younger patients?
Lymphoid hyperplasia is thought to be common cause in younger patients
Most common etiology of acute appendicitis in older patients?
Blockage by solid particles of stool fecaliths is more common etiology in adults
Pathophysiology of acute appendicitis?
Obstruction of appendiceal lumen (lymph node hyperplasia, fecalith, etc.) > continued mucus secretion and bacterial overgrowth > increased intraluminal pressure/inflammation/edema > venous congestion and impaired arterial flow = appendiceal ischemia > gangrene, necrosis, perforation, with irritation of parietal peritoneum
Signs and symptoms of acute appendicitis?
- Vague pain, initially epigastric or periumbilical
- Anorexia, nausea (comes after the pain), rarely vomiting
- Over course of 24 hours or less, pain intensifies and localizes to RLQ (visceral pain – somatic pain caused from parietal peritoneum)
- McBurney’s Point: maximal tenderness 2/3 of the distance from umbilicus to the right ASIS
- If patient complains of high fever, chills and describes pain that briefly subsided before getting worse, suspect a perforated appendix
Ddx of acute appendicitis?
- Gastroenteritis, Meckel’s diverticulitis, UTI and Crohn’s
- Women who are sexually active and of childbearing age - include ectopic pregnancy, pelvic inflammatory disease, ruptured ovarian cyst, tubo-ovarian abscess and ovarian torsion
- Older patients - include diverticulitis and malignancy
- Young children - include mesenteric adenitis and intussusception
Complication of acute appendicitis?
Appendiceal wall necrosis and translocation (gangrenous appendicitis) > Perforation and spillage of appendiceal contents > Peritonitis > Hemodynamic instability, sepsis, abdominal/appendiceal abscess
What is a missed appendicitis?
When a patient does not seek care within 24h after developing appendicitis-like symptoms, a diagnosis of ‘missed appendicitis’ is provided
Pathophysiology of missed appendicitis?
Omentum covers the area of inflammation and walls it off in the right iliac fossa. The infection will carry on and create an abscess or phlegmon
Symptoms of missed appendicitis?
A few days of pain, sometimes 7-10 days. Some days may be worse than others
Management of missed appendicitis?
- If sick, toxic, febrile, high WBC than surgery will probably be considered
- Most don’t require immediate surgery, usually admit for antibiotics, analgesia and sometimes PERC drain
- Recurrence is about ¼ if the appendix is not removed
- May want to get a barium enema or colonoscopy to ensure no Crohn’s disease
- Interval day surgery will be booked if the patient wants an appendectomy
Indications for urgent appendectomy?
Perforated and/or complicated appendicitis +/- hemodynamic instability, sepsis, free perforation, persistent abdominal pain, fever, and clinical signs of localized or diffuse peritonitis – especially if leukocytosis is present; for acute nonperforated appendicitis, immediate appendectomy should be performed within 12 hours of diagnosis – moreover, those with appendiceal abscess (especially if not amenable to percutaneous drainage)
Prophylactic antibiotics to use for acute appendicitis?
Ideally, at least 60 minutes before surgery – ceftriaxone 2g daily, flagyl 500mg BID
Investigations for acute appendicitis?
CBC (neutrophil shift) + Lytes + BUN (vomiting) + Creatinine + ALT (should be normal, r/o acute hepatitis) + Bilirubin + Lipase (r.o pancreatitis) + Urinalysis (r/o kidney stones)+ b-HCG (urine dip +/- serum r/o ectopic pregnancy)) + ECG + Abdominal Series X-rays
Imaging for acute appendicitis?
U/S (for appendicitis – useful to r/o gyne pathology in women; assess if there was periappendiceal fluid, surrounding inflammation + fat stranding, is there is dilation >6mm? – can do a dynamic study to see if compressible or if there is an echogenic fecalith present) + CT Scan w/contrast (can help diagnose an atypical presentation – all patients >50 should receive one unless unstable) The appendix is located just above the psoas muscle
Functional/non-mechanical cause of bowel obstruction?
Ileus – impaired bowel motility. Common causes: opiates, electrolytes abnormalities (hypokalemia) or intra-abdominal infections
Common mechanical SBO causes?
- Intraluminal: intussusception, gallstones, Bezoars
- Intramural: Crohn’s disease, radiation stricture, adenocarcinoma
- Extramural: previous surgery adhesions (75% of SBO), incarcerated hernia, peritoneal carcinomatosis
Symptoms & signs of SBO?
- Colicky pain (at first) > abdominal pain huge, ^HR, localized tender, leukocytosis, lactate acidosis (if strangulated)
- Diarrhea
- Early nausea, vomiting (more proximal > distal) – if feculent, then more established BO b/c of bacterial overgrowth
- Constipation, obstipation (no passage of stool or gas) – WHEN WAS THE LAST TIME THEY PASSED GAS
- Abdominal distention
- Tympany to percussion in central abdomen
- Hyperactive bowel sounds precedes absent bowel sounds
Findings on AXR for SBO?
Proximal dilated SB (>3cm in diameter), air fluid levels on upright film (LADDER APPEARANCE) – if its just 2 lines, then probably an ileus, no colonic gas. If there is fluid-filled loops – string of beads
Risk factors for SBO?
Prior abdominal surgery or presence of abdominal wall hernias
Labs for SBO?
- Creatinine + HCT: assess degree of hydration. Hemoconcentration indicated by elevated hemoglobin and hemocrit
- Electrolyte Abnormalities: may see this and metabolic hypochloremic alkalosis due to frequent emesis
- Amylase: elevated. You should not see an elevation of lipase. Amylase and lipase-done to rule out pancreatitis. Should be normal in a patient with bowel obstruction or only have a mild elevation of amylase
- CBC: leukocytosis + ^lactate (late sign) – both of these if strangulation
Indications for emergency operation for SBO?
Peritonitis, high fever or high concern of ischemia, elevated white blood count, primary SBO (tumor) – all those that shouldn’t have adhesions
Indications of surgery for SBO?
If no improvement or worsening sx after trial of conservative management then surgery is indicated. Complete obstruction, closed loop obstruction, perforation or dead gut
Non-operative management of SBO?
NPO, NG tube, resuscitation (IV isotonic fluids, foley catheter and serial abdominal exams), gastrografin. 50% resolve their sx
- Overall: IV isotonic fluid resuscitation + urine output monitoring with catheter + 10mg buscopan (relaxes the bowels), and gravol
- NG Tube for Gastric Decompression: decreases nausea, distention, risk of aspiration from vomiting
Complications of SBO?
Ischemia, perforation, toxic megacolon (septic patient with exceedingly dilated colon – 12cm: IBD, c.dif, pseudo-obstruction, mechanical obstruction, volvulus), closed loop obstruction (both ends of the obstructed segment are blocked)
Common mechanical LBO causes?
- Intraluminal: constipation, foreign bodies
- Intramural: adenocarcinoma, diverticulitis, IBD stricture, radiation stricture
- Extramural: volvulus, adhesions, hernias (sigmoid colon in inguinal groin hernia)
Signs and symptoms of LBO?
Nausea/vomiting, colicky abdo pain, distention, constipation, bowel sounds normal/increased/absent if ileus
Pathophysiology of open loop LBO?
Incompetent ileocecal valve allows relief of colon pressure as contents reflex INTO the ileum > clinical features are similar to SBO
Pathophysiology of closed loop LBO?
Competent ileocecal valve results in proximal/distal occlusions and massive colonic distention then pressure in the cecum > bowel wall ischemia > necrosis > perforation
What is functional/acute-pseudo obstruction?
Distention of colon without actual obstruction in distal end – exact mechanism unknown; ends up leading to abdominal distention (acute/gradual over 3-7d), abdominal pain, nausea, vomiting, constipation, diarrhea, fever, leukocytosis, peritoneal signs
Findings on AXR for LBO?
Dilated LB, primarily cecum (>9cm in diameter), more than 12cm is a risk for perforation, air fluid levels (PICTURE FRAME APPEARANCE) + proximal distention/distal decompression, no small bowel air if competent ileocecal valve – Coffee Bean Sign (i.e. sigmoid volvulus)
Treatment of mechanical LBO?
Surgical correction of obstruction, usually resection and diverting colostomy – volvulus requires sigmoidoscopic/endoscopic decompression first, then if not, operative resection
Treatment of functional LBO?
Treat underlying cause, NPO, nasogastric tube decompression (or rectal tube decompression, colonoscopy, neostigmine), or surgical decompression (ostomy/resection) uncommon
What is paralytic ileus?
Temporary, reversible impairment of intestinal motility, most frequently caused by = abdominal operations, infections/inflammation, medications (opiates, anesthetics, psychotropics), electrolyte abnormalities
Signs and symptoms of paralytic ileus?
Same as mechanical obstruction but without actual obstruction – however, bowel sounds are diminished/absent, not hyperactive; post-op gastric/SB motility returns by 24-48hrs, colonic motility by 3-5d
Investigations of paralytic ileus?
Routine post-op ileus is expected, so no investigations required; if persists or without abdominal surgery, then review patient medications (opiates), monitor serum electrolytes (+ magnesium, calcium, phosphate), CT scan to r/o abscess/peritoneal sepsis or exclude complete mechanical obstruction
Treatment of paralytic ileus?
NPO + fluid resuscitation + nasogastric decompression + correct causative abnormalities (e.g. sepsis, meds, electrolytes), consider TPN for prolonged ileus
Etiology of intestinal ischemia?
Arterio-occlusive mesenteric ischemia (thrombotic, embolic, extrinsic compression [strangulating hernia]), non-occlusive mesenteric ischemia (mesenteric vasoconstriction 2˚ to systemic hypoperfusion [preserves supply to vital organs]), mesenteric venous thrombosis (consider hypercoagulable state, DVT)
Signs and symptoms of intestinal ischemia?
Acute – severe abdo pain out of proportion to physical, vomiting, bloody diarrhea, bloating, minimal peritoneal signs, hypotension, shock, sepsis; chronic – postprandial pain, fear of eating, weight loss
Labs for intestinal ischemia?
Leukocytosis (nonspecific) + lactic acidosis (late finding) + get amylase/lactate/CK/ALP (observe progress) + hypercoagulability workup if suspect venous thrombosis
Imaging findings of intestinal ischemia?
- ABDO XR: portal venous gas, intestinal pneumatosis, free air if perforation
- CONTRAST CT: thickened bowel wall, luminal distention, SMA or SMV thrombus, mesenteric or portal venous gas and pneumatosis
- CT ANGIO: GOLD STD for acute arterial ischemia
Treatment of intestinal ischemia?
- Fluid resuscitation – correct the metabolic acidosis, NPO, nasogastric decompression of the stomach + prophylactic broad-spectrum ABX
- Surgery: exploratory laparotomy +/- angiogram, embolectomy/thrombectomy, bypass/graft, mesenteric endarterectomy, anticoagulation therapy, percutaneous transluminal angioplasty ± stent + segmental resection of necrotic intestine
Etiology of abdominal distension
- Ascites
- Portal HTN – Cirrhosis, Cardiac failure, Hepatic vein thrombosis
- Normal Portal HTN - Cancer (especially ovarian), Pancreatitis, TB - Flatulence
- Functional bowel disease (e.g. IBS)
- Fibre
- Lactose intolerance
- Chewing gum (e.g. sorbitol, mannitol) - Feces
- Constipation
- Colonic obstruction
- Dysmotility - Other
- Pregnancy (fetus)
- Obesity (fat)
- Blood
- Large tumours (fatal growth)
Differential diagnosis of abdominal distention
6Fs: Fat, Feces, Fetus, Flatus, Fluid, Fetal Growth
DDx of weight loss?
- Psychiatric/Neurologic disease – depression, dementia, stroke, Parkinson’s disease, eating disorder
- Endocrine/Metabolic – hyperthyroidism, DM, hyperparathyroidism
- GI – malabsorption (celiac disease, CF), PUD, IBD
- Cardiac – CHF
- Respiratory – COPD, and other respiratory diseases
- Renal – end stage renal failure
- Infections – HIV, TB, chronic HCV, fungal
- Rheumatologic disease – lupus, RA, GCA
- Malignancy – GI, lung, lymphoma, prostate
Investigations of weight loss?
- Blood work: CBC, lytes, liver enzymes, CRP, Cr, urea, albumin, INR, total protein, TSH, fasting blood glucose, HIV serology, hep B/C serology, anti-TTG + IgA level, vit B12, iron studies
- Imaging: CXR, abdominal US
- Cancer screening: mammography, FIT/colonoscopy, pap smear, PSA
- MMSE
- Geriatric Depression Scale
