Gastroenterology

Question 1

What anatomical landmark is used to classify upper vs lower GI bleeds?

Answer 1

Ligament of Treitz

Question 2

What are the causes of UGIB?

Answer 2

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

Question 3

Which investigations should be done for UGIB?

Answer 3

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

Question 4

What percentage of GI bleeds stop spontaneously?

Answer 4

80%

Question 5

Medical treatment of UGIB?

Answer 5

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

Question 6

Two most common procedures endoscopically for UGIB?

Answer 6

epi injection therapy + thermal

Question 7

What should you consider to accelerate gastric emptying prior to gastroscopy to remove clots from stomach?

Answer 7

IV erythromycin

Question 8

Acute treatment of esophageal varices?

Answer 8

IV Octeotride (somatostatin analogue that decreases splanchnic blood flow/portal pressure), endoscopic therapy: variceal ligation or sclerotherapy.

Question 9

Longterm treatment of esophageal varices?

Answer 9

B-blocker, nitrates, repeat EVL/sclerotherapy

Question 10

Persistent/recurrent treatment of esophageal varices?

Answer 10

TIPS (transhepatic internal portal shunt – risk is that you bypass blood over liver and lose detox). Blakemore tube

Question 11

Causes of LGIB?

Answer 11

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

Question 12

What type of bleeding for LGIB results in unchanged bowel habits?

Answer 12

Anal bleeding

Question 13

What is angiodysplasia?

Answer 13

Vascular malformation (focal submucosal venous dilatation or tortuosity)

Question 14

Physical for Rectal Bleeding/Altered Bowel Habit?

Answer 14

Abdo exam EDAP (External, digital, anoscopy, proctoscopy)

Question 15

Investigations for LGIB?

Answer 15

● >50yo + bleeding > colonoscopy (if with red flags urgently)
● <50yo + bleeding > rigid or flexible sigmoidoscopy/barium enema

Question 16

If LGIB and you have increased suspicion of UGIB what should you order?

Answer 16

colonoscopy + gastroscopy

Question 17

For slow LGIB investigations?

Answer 17

For SLOW bleeding (<0.5mL/min) > Radionucleotide Tc-99m-tagged RBC scan

Question 18

For rapid LGIB investigation?

Answer 18

For RAPID bleeding (>0.5mL/min) > Angiography ± Embolization

Question 19

Dysphagia can be thought of in two categories.

Answer 19

Oropharyngeal and esophageal

Question 20

Symptoms of oropharyngeal dysphagia

Answer 20

Nasal regurg, difficulty initiating swallow, choking/coughing. Perhaps some associated neuro symptoms

Question 21

3 broad causes of oropharyngeal dysphagia?

Answer 21

1. Neurological
2. Muscular
3. Structural

Question 22

Neurological causes of oropharyngeal dysphagia?

Answer 22

MS, stroke

Question 23

Muscular causes of oropharyngeal dysphagia?

Answer 23

polymyositis, myasthenia gravis, muscular dystrophy

Question 24

Structural causes of oropharyngeal dysphagia?

Answer 24

Zenker’s diverticulum, thyromegaly/goiter, cervical spur, tumor

Question 25

Investigations for oropharyngeal dysphagia?

Answer 25

Neurological exam + Cine swallow

Question 26

Esophageal dysphagia can be broken up into.

Answer 26

Mechanical and motor

Question 27

Mechanical obstruction primarily affects solids or liquids

Answer 27

Solids

Question 28

Motor dysphagia primarily affects solids or liquids

Answer 28

Both

Question 29

Examples of intermittent mechanical dysphagia

Answer 29

Lower esophageal rings/webs - Schatski’s ring

Question 30

Symptoms of mechanical dysphagia?

Answer 30

SOLIDS worse than liquids. Not temp sensitive, regurg of boluses

Question 31

Examples of progressive mechanical dysphagia

Answer 31

If age >50 and associated weight loss - cancer. If heartburn associated peptic stricture

Question 32

Investigations for mechanical causes of dysphagia.

Answer 32

Barium swallow, endoscopy (+/- biopsy)

Question 33

Symptoms of motor dysphagia

Answer 33

Gradual onset, liquids and solids both affected, temp sensitive

Question 34

Examples of intermittent motor dysphagia

Answer 34

Diffuse esophageal spasm

Question 35

What symptom/s would make you think of diffuse esophageal spasm.

Answer 35

Spontaneous chest pain that radiates to the back + GER

Question 36

Triad for achalasia

Answer 36

Weight loss, regurg undigested food and dysphagia

Question 37

Examples of progressive motor dysphagia

Answer 37

Achalasia, scleroderma (reflex symptoms)

Question 38

Investigations for motor dysphagia

Answer 38

Barium swallow, esophageal manometry

Question 39

Classic bird’s beak narrowing

Answer 39

Achalasia

Question 40

Which enzymes are indicators of hepatocyte damage?

Answer 40

ALT and AST

Question 41

Which enzymes are indicators for bile duct damage?

Answer 41

ALP and GGT

Question 42

Which liver enzyme is more specific to liver damage?

Answer 42

ALT

Question 43

What is the most common cause of increased ALT?

Answer 43

Fatty liver

Question 44

What can increase an AST?

Answer 44

Liver damage, kidney, brain, RBC and muscle (rhabdomyolysis, MI, extensive surgery, PE)

Question 45

DDx for increased ALT/AST

Answer 45

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)

Question 46

AST/ALT ratio of <1

Answer 46

Viral or autoimmune hepatitis (chronic liver disease)

Question 47

AST/ALT ratio of >2

Answer 47

EtOH liver disease or biliary obstruction

Question 48

AST/ALT ratio of >4

Answer 48

Wilson’s Disease

Question 49

What do you use to assess biliary function?

Answer 49

Serum bilirubin, serum albumin, ALP, GGT

Question 50

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

Answer 50

Pale, bulky and more difficult to flush.

Question 51

Examples of unconjugated hyperbilirubinemia

Answer 51

Haemolysis (e.g. haemolytic anaemia)
Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)
Impaired conjugation (e.g. Gilbert’s syndrome)

Question 52

Examples of conjugated hyperbilirubinemia

Answer 52

Hepatocellular injury

Cholestasis

Question 53

Causes of increased ALP?

Answer 53

Cholestasis, bone growth (Paget’s disease, osteoblastic cancers – breast) placenta , anabolic steroids

Question 54

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

Answer 54

• Bony metastases or primary bone tumours (e.g. sarcoma)
• Vitamin D deficiency
• Recent bone fractures
• Renal osteodystrophy

Question 55

What to use to assess liver synthetic function (the last two things to go)?

Answer 55

PT and serum blood glucose

Question 56

Common causes of large duct cholestasis

Answer 56

• Benign (stricture, stones, primary sclerosing cholangitis (MOST COMMON)),
• Malignant (GB ca, ampullary ca, pancreatic ca)

Question 57

Common causes of small duct cholestasis

Answer 57

• 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)

Question 58

What is sialadenitis?

Answer 58

Inflammation of the salivary glands

Question 59

Typical presentation of sialadenitis?

Answer 59

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

Question 60

Lab features of sialadenitis?

Answer 60

Lab features: high serum amylase

Question 61

What causes sialadenitis?

Answer 61

Cause: usually bilateral (sometimes unilateral) inflammation of the salivary glands caused by mumps virus (usually Paramyxovirus) OR bacteria (often staph aureus).

Question 62

Treatment of sialadenitis?

Answer 62

Treatment: supportive if viral. Complications can affect postpubertal male testicles causing epididymitis → sterility. If bacterial – treat with cloxacillin ± abscess drainage, sialogogues

Question 63

What is the definition of sialolithiasis?

Answer 63

Presence of calculi/stones in salivary glands or ducts

Question 64

What gland does sialolithiasis usually occur?

Answer 64

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

Question 65

What is the common presentation of sialolithiasis?

Answer 65

Pain in gland region especially when eating ± swelling near submandibular region. About 33% present with painless swelling. Usually unilateral.

Question 66

Investigations for sialolithiasis?

Answer 66

Can show up on X-ray, but up to 20% not detected on X-ray. Can try sialogram (inject dye and film duct system).

Question 67

Management of sialolithiasis?

Answer 67

• 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.

Question 68

Risk factors for xerostomia?

Answer 68

Risk factors for this includes age and medication use

Question 69

What is xerostomia?

Answer 69

Mouth dryness or mucinous quality saliva

Question 70

Causes of xerostomia?

Answer 70

Causes: anticholinergic action of systemic medications, radiation for head/neck cancer, Sjogren’s syndrome

Question 71

Presentation of xerostomia

Answer 71

Presentation: messed up taste, dry mouth or mucous mouth, infection, dental caries (saliva acts as a buffer)

Question 72

Management of xerostomia?

Answer 72

Management: review meds, dental measures, substitute or stimulate saliva with ACh analogues (e.g. Pilocarpine).

Question 73

What is Sjogren’s syndrome?

Answer 73

Autoimmune injury to salivary + lacrimal glands (incurable)

Question 74

What are the most common diseases associated with secondary Sjogren’s?

Answer 74

The most common diseases associated with SS are rheumatoid arthritis and systemic lupus erythematosus.

Question 75

What is presentation of sicca syndrome?

Answer 75

Presentation: dry eyes and mouth, possible swelling of glands usually bilaterally.

Question 76

What is the risk of primary Sjogren’s

Answer 76

Malignant lymphoma developing in salivary glands

Question 77

When should Sjogren’s syndrome be suspected

Answer 77

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).

Question 78

Treatment of Sjogren’s syndrome?

Answer 78

Incurable, maybe monoclonal antibodies, saliva substitutes or stimulants (Salagen)

Question 79

What is a mucocoele?

Answer 79

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.

Question 80

Presentation of mucocoele?

Answer 80

Presentation: Hx: minor trauma, esp. lower lip usually in young children and adults

Question 81

What is the standard management of mucocele?

Answer 81

Remove associated minor gland. Surgical removal of the entire lesion and histologic confirmation of clinical diagnosis is the standard management of mucocele

Question 82

What treatment option should not be done for mucoceles?

Answer 82

No Tx with lancing

Question 83

What causes cheilitis?

Answer 83

Excess sun exposure. It can also be a sign of iron deficiency.

Question 84

What is cheilitis?

Answer 84

Cheilitis is an acute or chronic inflammation of the lips characterized by dryness, scaling, erythema, and fissuring of the lips.

Question 85

Before making the diagnosis of burning mouth syndrome, what should you exclude

Answer 85

Exclude other mucosal diseases, including xerostomia and allergic contact stomatitis.

Question 86

What is burning mouth syndrome and who does it primarily affect?

Answer 86

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.

Question 87

Treatments for burning mouth syndrome?

Answer 87

Treatments for burning mouth syndrome include tricyclic antidepressants, benzodiazepines, and gabapentin.

Question 88

Most common gland for salivary gland neoplasm?

Answer 88

Cause: esp. parotid gland (80-85%) but majority benign

Question 89

What percentage of minor salivary gland tumors are malignant?

Answer 89

> 50% minor salivary gland tumors are malignant

Question 90

Treatment of minor salivary gland tumors?

Answer 90

Tx: wide excision

Question 91

What is the most common cause of mouth ulcers.

Answer 91

Recurrent aphthous stomatitis

Question 92

What are aphthous stomatitis (Canker sores)?

Answer 92

Aphthae are painful oral lesions that appear as localized, shallow, round to oval ulcers with a yellowish adherent exudate centrally.

Question 93

What causes aphthous stomatitis (Canker sores)?

Answer 93

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.

Question 94

In most individuals when do aphthous stomatitis (Canker sores) resolve?

Answer 94

In most individuals, they resolve in 10 to 14 days

Question 95

List three associated conditions of aphthous stomatitis (Canker sores).

Answer 95

Celiac + crohn’s, behcet’s syndrome (Triad of oral, genital, and eye ulcers)

Question 96

Behcet’s Syndrome triad

Answer 96

Triad of oral, genital, and eye ulcers

Question 97

Behçet syndrome is believed to be due to ____?

Answer 97

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.

Question 98

_______ the most specific lesion for Behçet syndrome, occurs in 75 percent or more of patients with Behçet syndrome

Answer 98

Genital ulceration, the most specific lesion for Behçet syndrome, occurs in 75 percent or more of patients with Behçet syndrome

Question 99

______ can be associated with canker sores – other manifestations include candidiasis, hairy leukoplakia, squamous cell carcinoma, Kaposi’s, or major ulcers.

Answer 99

HIV/AIDS can be associated with canker sores – other manifestations include candidiasis, hairy leukoplakia, squamous cell carcinoma, Kaposi’s, or major ulcers.

Question 100

Treatment for recurrent aphthous stomatitis

Answer 100

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

Question 101

Early childhood caries are an infectious disease caused by ____

Answer 101

Early childhood caries are an infectious disease caused by strep mutans

Question 102

What population/s does early childhood caries affect more?

Answer 102

Affects low income/Aboriginals more

Question 103

How can you prevent early childhood caries?

Answer 103

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.

Question 104

Treatment of early childhood caries?

Answer 104

• Extracted are by expanding the socket, severing the periodontal ligament
• Stainless steel crowns

Question 105

Risk factors for oral squamous cell carcinoma?

Answer 105

Risk factors: sun exposure, smoking, alcohol

Question 106

What are considered pre-malignant lesions for oral squamous cell carcinoma?

Answer 106

Pre-malignant lesions (i.e. leukoplakia or erythroplakia)

Question 107

Appearance of oral squamous cell carcinoma?

Answer 107

Cancers are often indurated and firm with a rolled border.

Question 108

How often is the oral mucosa involved in lichen planus?

Answer 108

The oral mucosa is involved in about 50% of cases

Question 109

Appearance of lichen planus (oral) and what are their hallmark feature?

Answer 109

Reticulated, lacy, bluish white, linear lesions (Wickham striae) are a hallmark of oral lichen planus, especially on the buccal mucosae.

Question 110

What are the two groups for oral cleft?

Answer 110

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.

Question 111

Treatment of oral cleft?

Answer 111

Tx: surgical repair

Question 112

Investigations for abdominal/pelvic mass?

Answer 112

• 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

Question 113

History for abdominal/pelvic mass?

Answer 113

• 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

Question 114

Physical exam for abdominal/pelvic mass?

Answer 114

• 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

Question 115

Etiology for abdominal/pelvic mass?

Answer 115

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

Question 116

Definition of constipation?

Answer 116

Infrequent passage of stools, passage of hard/small stool, excess straining during defecation or sense of incomplete bowel evacuation

Question 117

2 categories of aetiologies constipation

Answer 117

1. Functional

2. Organic

Question 118

What are the aetiologies of functional constipation?

Answer 118

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)

Question 119

What are the aetiologies of organic constipation?

Answer 119

• 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

Question 120

Clinical features of constipation?

Answer 120

Stool firm, difficult to expel, passed with straining, abdominal pain relieved by defecation, flatulence

Question 121

Red flags of constipation?

Answer 121

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

Question 122

How to calculate constipation score?

Answer 122

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

Question 123

Bristol stool chart

Answer 123

1: like rabbit droppings 2: grapes 3: corn on cob 4: sausage 5: nugs 6: porridge 7: gravy

Question 124

What investigation should be ordered if concomitant symptoms such as rectal bleeding, weight loss, anemia or age above 50 in constipation?

Answer 124

Colon visualization (colonoscopy, CT colonography)

Question 125

What physical exam should you do for chronic constipation?

Answer 125

RECTAL EXAM (anal wink reflex, observe perineal descent on bearing down, resting tone, squeeze pressure).

Question 126

What are the investigations if constipation is the only presenting symptom?

Answer 126

• 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

Question 127

If therapeutic trial does not work for constipation what should be your next steps?

Answer 127

Send for colonic transit or anorectal manometry if normal, or barium/MR defecography in unsure. NO COLONOSCOPY unless >50 or alarm features.

Question 128

What are the examples of surfactants in the treatment of constipation and how do they work?

Answer 128

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

Question 129

What is the patient education and dietary changes to recommend in the treatment of constipation?

Answer 129

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

Question 130

What are the examples of osmotic agents in the treatment of constipation and how do they work?

Answer 130

 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

Question 131

What are the examples of stimulant agents in the treatment of constipation and how do they work?

Answer 131

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.

Question 132

What is the treatment for severe constipation?

Answer 132

• 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.

Question 133

What is the definition of diarrhea?

Answer 133

Increased stool liquidity + weight (more than 300 g/day), increased stool frequency (>3/day)

Question 134

What are the symptoms of diarrhea?

Answer 134

Associated with urgency, abdominal cramps, and incontinence

Question 135

What is the definition of acute diarrhea and when does it resolve?

Answer 135

(<2 wks) is usually infectious (90%), a drug side effect, or a toxin. Usually self-limiting + resolve within 7d.

Question 136

Risk factors for acute diarrhea?

Answer 136

Raw or undercooked meat/seafood, unpasteurized dairy products, antibiotics/laxatives, high risk sexual activity, infectious outbreaks, family history (IBD), occupational exposures

Question 137

Acute diarrhea can be broken up into 2 types?

Answer 137

• Non-inflammatory (Watery)

- Inflammatory

Question 138

Etiology of non-inflammatory (watery) acute diarrhea?

Answer 138

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

Question 139

Symptoms of inflammatory acute diarrhea?

Answer 139

Bloody (not always), Small volume, high frequency, Often lower abdominal cramping with urgency ± tenesmus. May have fever ± shock

Question 140

Investigations for inflammatory acute diarrhea?

Answer 140

Fecal WBC and RBC positive

Question 141

Pathophysiology of inflammatory acute diarrhea and what part of the bowel does it affect?

Answer 141

• Organisms and cytotoxins invade mucosa, killing mucosal cells, and further perpetuating the diarrhea
• Usually colon

Question 142

Etiology of inflammatory acute diarrhea?

Answer 142

Salmonella, Shigella, Campylobacter – most common, E Coli 0157H:7, Yersinia. (SECSY). Others: NSAIDs, IBD, ischemic

Question 143

What is the definition of chronic diarrhea?

Answer 143

> 4wks, rarely infectious/parasitic (exceptions are Giardiasis, C. Difficile)

Question 144

What are the 4 categories of chronic diarrhea?

Answer 144

1. Osmotic
2. Secretory
3. Inflammatory
4. Abnormal motility

Question 145

Pathophysiology of osmotic chronic diarrhea?

Answer 145

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

Question 146

Etiology of osmotic chronic diarrhea?

Answer 146

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.

Question 147

S&S of osmotic chronic diarrhea?

Answer 147

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

Question 148

Pathophysiology of secretory chronic diarrhea?

Answer 148

Loss of fluids + electrolytes from intestine

Question 149

Etiology of secretory chronic diarrhea?

Answer 149

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

Question 150

S&S of secretory chronic diarrhea?

Answer 150

Diarrhea persists despite fasting, minimal cramps and pain, large volume watery stools, absence of mucus, blood, or excess fat in the stool

Question 151

Pathophysiology of inflammatory chronic diarrhea?

Answer 151

Some kind of damage to gut villi = breakdown of cells = activated inflammatory mediators

Question 152

Etiology of inflammatory chronic diarrhea?

Answer 152

Invasive infections (Salmonella, Shigella, E.coli 0157H:7, Campylobacter, Yersinia), radiation therapy, IBD (UC or Crohn’s)

Question 153

S&S of inflammatory chronic diarrhea?

Answer 153

Systemic symptoms like fever, fatigue, night sweats, weight loss; visible blood in stools, significant cramps and pain, PMN’s on stool microscopy

Question 154

Pathophysiology of abnormal motility chronic diarrhea?

Answer 154

Reduced transit time leads to decreased water absorption.

Question 155

Etiology of abnormal motility chronic diarrhea?

Answer 155

IBS, hyperthyroidism, post-surgical diarrhea (vagotomy, resection of ileocecal valve)

Question 156

S&S of abnormal motility chronic diarrhea?

Answer 156

Stools tend to be soft, porridge-like

Question 157

Compare organic vs functional diarrhea

Answer 157

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.

Question 158

What causes traveller’s diarrhea and how can it be prevented?

Answer 158

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).

Question 159

What are you concerned about if prior antibiotic use for etiology of diarrhea?

Answer 159

C Difficile (get pseudomembranous colitis)!

Question 160

What are you concerned about if HIV for etiology diarrhea?

Answer 160

Opportunistic infections (Cryptosporidia, CMV)or lymphoma

Question 161

History for diarrhea?

Answer 161

Travel, homosexual contacts, outbreaks, seafood, extraintestinal signs of IBD, FHx, antibiotics, diet, steatorrhea, weight loss, immunosuppressed, laxatives, tumor history , sexual history

Question 162

Investigations for acute diarrhea?

Answer 162

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

Question 163

Investigations for chronic diarrhea?

Answer 163

• 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

Question 164

DO NOT empirically prescribe anti-diarrheal especially with _______

Answer 164

Fever or hematochezia

Question 165

Are antibiotics generally required for the treatment of diarrhea?

Answer 165

Generally not required unless pt high risk or has severe Sx (>6 episodes/day, hematochezia, febrile > 1wk)
Most cases are self limiting

Question 166

First step to management of diarrhea?

Answer 166

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

Question 167

Antibiotic for C. difficile and duration?

Answer 167

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

Question 168

Antibiotic for Giardia?

Answer 168

Metronidazole

Question 169

Antibiotic for Salmonella, Campylobacter, E.col?

Answer 169

Cipro

Question 170

MOA of opioids (antidiarrheal)?

Answer 170

Activation of δ receptors = reduced secretory activity + mew receptors = enhanced NaCl + water absorption = net effect of reduction of fluid entering the large intestines

Question 171

MOA of absorbants (antidiarrheal)?

Answer 171

Act by absorbing intestinal toxins/micro-organisms or by coating intestinal mucosa

Question 172

Examples of modifiers of fluid transport (antidiarrheal)?

Answer 172

Bismuth subsalicylate (Pepto-Bismol)

Question 173

Examples of opioids (antidiarrheal)?

Answer 173

Methylnatrexone or alvimopan. If you constipate someone with too much opioid, reverse with these.

Question 174

Prevention in Traveler’s diarrhea?

Answer 174

• 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

Question 175

Examples of absorbants (antidiarrheal)?

Answer 175

Kaolin/pectin (Kaopectate), methylcellulose, activated attapulgite

Question 176

Side effects of anti-motility agents?

Answer 176

Side Effects: abdo cramps, toxic megacolon

Question 177

Examples of anti-motility agents?

Answer 177

Diphenoxylate, loperamide (Imodium)

Question 178

Contraindications to anti-motility agents?

Answer 178

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

Question 179

4 types of antidiarrheal?

Answer 179

• Anti-Motility Agents
• Absorbants
• Modifiers of Fluid Transport
• Opioids

Question 180

What is GERD?

Answer 180

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.

Question 181

What are the causes of GERD?

Answer 181

Obesity (increased abdo pressure), lower esophageal sphincter pressure, decreased esophageal peristalsis, gastric acid hypersecretion (Zollinger-Ellison syndrome), delayed gastric emptying, and overeating

Question 182

What are the risk factors of GERD?

Answer 182

EtOH, nicotine, obesity, dietary fat, peppermint, meds (narcotics, Ca2+ channel blockers, aspirin and NSAIDS), hormones (estrogen, glucagon)

Question 183

What are the typical symptoms of GERD?

Answer 183

• 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

Question 184

What should be asked on HPI for GERD?

Answer 184

• 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)

Question 185

What medications can cause GERD?

Answer 185

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

Question 186

Physical exam for GERD?

Answer 186

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

Question 187

How is GERD diagnosed?

Answer 187

• 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

Question 188

What are some indications that testing is required for GERD and what are the options?

Answer 188

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

Question 189

What are some of the alarm symptoms that should be asked on history?

Answer 189

• 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

Question 190

____ is indicated in patients who have a normal gastroscopy but with chest pain and/or dysphagia?

Answer 190

Esophageal manometry

Question 191

What is the Ddx for GERD?

Answer 191

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

Question 192

_______ which may account for up to 90% of patients reporting heartburn refractory to twice-daily proton pump inhibitors

Answer 192

Functional esophageal disorders

Question 193

What is functional heartburn?

Answer 193

Reflux hypersensitivity, characterized by normal esophageal acid exposure but a positive (> 95%) symptom association probability (SAP) for acid reflux or nonacid reflux.

Question 194

Complications of GERD?

Answer 194

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.

Question 195

What are the lifestyle treatment options for GERD?

Answer 195

Dietary (avoid fat, caffeine), avoid eating 4h before bed, smoking, elevate head of bed (6-9 in), weight loss, avoid tight fitting clothes.

Question 196

What are the medical treatment options for GERD?

Answer 196

 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

Question 197

What are the surgical options for GERD?

Answer 197

Surgery: Nissen fundoplication – gastric fundus is wrapped around the LES strengthening junction

Question 198

What is the definition of Barrett’s esophagus?

Answer 198

Metaplasia of normal squamous esophageal epithelium to intestinal columnar epithelium containing- type intestinal mucosa (intestinal metaplasia)

Question 199

Etiology of Barrett’s esophagus?

Answer 199

Thought to be acquired via long-standing GERD and consequent damage to squamous epithelium

Question 200

Barrett’s esophagus is more common in who?

Answer 200

More common in males, age >50, Caucasians, smokers, overweight, hiatus hernia, and long history of reflux symptoms

Question 201

Diagnosis of Barrett’s esophagus?

Answer 201

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

Question 202

Treatment of Barrett’s esophagus?

Answer 202

o Acid suppressive therapy with high-dose PPI indefinitely (or surgical fundoplication)
o Surveillance gastroscopy every 3yr if no dysplasia

Question 203

Treatment if high grade dysplasia (Barrett’s esophagus)?

Answer 203

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

Question 204

Treatment if low grade dysplasia (Barrett’s esophagus)?

Answer 204

If low grade dysplasia, both surveillance (every 6mo for 1yr then annually) and endoscopic ablation/resection are satisfactory options

Question 205

Worrisome features of anorectal pain?

Answer 205

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

Question 206

Physical for rectal bleeding/altered bowel habit?

Answer 206

1. Abdo exam
2. 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

Question 207

Etiology of rectal bleeding/altered bowel habit?

Answer 207

• 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

Question 208

Investigations of rectal bleeding/altered bowel habit?

Answer 208

• 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

Question 209

Signs and symptoms of IBD as anorectal pain?

Answer 209

Purulent discharge, Pain in the rectum (sometimes) and/or abdomen (often), Sometimes draining fistula, Sometimes diarrhea

Question 210

Risk factors of hemorrhoids?

Answer 210

^intra-abdominal pressure (chronic constipation, pregnancy, obesity, portal HTN, heavy lifting)

Question 211

Etiology of hemorrhoids?

Answer 211

• 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

Question 212

Internal hemorrhoids symptoms?

Answer 212

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

Question 213

What is 1st degree internal hemorrhoid?

Answer 213

1st Degree: bleed but do not prolapse through anus

Question 214

Treatment for 1st degree internal hemorrhoid

Answer 214

High fibre/bulk diet, sitz bath, steroid cream, pramoxine (Anusol, hydrocortisone, preparation H), rubber bad ligation, sclerotherapy, photocoagulation

Question 215

What is 2nd degree internal hemorrhoid?

Answer 215

2nd Degree: bleed, prolapse with straining, spontaneous reduction

Question 216

Treatment for 2nd degree internal hemorrhoid

Answer 216

Treatment: rubber band ligation, photocoagulation

Question 217

What is 3rd degree internal hemorrhoid?

Answer 217

3rd Degree: bleed, prolapse, requires manual reduction

Question 218

Treatment for 3rd degree internal hemorrhoid

Answer 218

Treatment: rubber band ligation (doesn’t work as well), or hemorrhoidectomy

Question 219

What is 4th degree internal hemorrhoid?

Answer 219

4th Degree: bleed, permanently prolapsed and cannot be manually reduced

Question 220

Treatment for 4th degree internal hemorrhoid

Answer 220

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

Question 221

Symptoms of external hemorrhoid

Answer 221

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

Question 222

Symptoms of dilated venules external hemorrhoid

Answer 222

Mildly symptomatic, pain after bowel movement, associated with poor hygiene, bleeding

Question 223

Treatment of dilated venules external hemorrhoid

Answer 223

Dietary fibre, stool softeners, steroid cream (short course), pramoxine (Anusol), avoid prolonged straining

Question 224

Symptoms of thrombosed external hemorrhoid

Answer 224

Very painful, more likely to bleed, resolve w/n 2wks, may leave perianal skin tag

Question 225

Treatment of thrombosed external hemorrhoid

Answer 225

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

Question 226

Definition of anal fissure?

Answer 226

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

Question 227

Pathophysiology of anal fissure?

Answer 227

Repetitive Injury after 1st Tear: sphincter spasm occurs preventing edges from healing and leads to further tearing, ischemia may ensure and contribute to chronicity

Question 228

Etiology of anal fissure?

Answer 228

• Local trauma: constipation, irritation, diarrhea, vaginal delivery, anal intercourse
• Secondary to: Crohn’s disease, granulomatous diseases, malignancy, communicable diseases

Question 229

Signs and symptoms of acute anal fissure?

Answer 229

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

Question 230

Signs and symptoms of chronic anal fissure?

Answer 230

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

Question 231

Treatment of acute anal fissure?

Answer 231

Acute: conservative – stool softeners, bulking agents, sitz bath, analgesia

Question 232

Treatment of chronic anal fissure?

Answer 232

• 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

Question 233

Pathophysiology of anorectal abscess?

Answer 233

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.

Question 234

The most common spaces involved in anorectal abscesses are ____ and _____, totaling 80% of presentations.

Answer 234

Perianal

Ischiorectal

Question 235

Causes of anorectal abscess?

Answer 235

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

Question 236

Common bacteria of anorectal abscess?

Answer 236

E. coli, proteus, streptococci, staphylococci, bacteriodes, anaerobes

Question 237

Signs and symptoms of anorectal abscess?

Answer 237

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

Question 238

Treatment of anorectal abscess?

Answer 238

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

Question 239

Definition of anal fistula?

Answer 239

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.

Question 240

Types of anal fistula?

Answer 240

1. Intersphincteric 40%
2. Trans-sphincteric 30% (through the external sphincter muscle).
3. Suprasphincteric 20% very rare
4. Extrasphincteric 10% - don’t start at the dentate line

Question 241

Etiology of anal fistula?

Answer 241

Same processes that lead to the formation of an anal abscess, others (post op, trauma, anal fissure, malignancy, radiation proctitis). **THINK ABOUT CROHN’S

Question 242

Signs and symptoms of anal fistula?

Answer 242

Intermittent or constant purulent d/c from perianal opening, pain, redness, tender, swelling, palpable cord-like tract, recurrent perirectal abscess

Question 243

What is Goodall’s rule?

Answer 243

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.

Question 244

When does Goodall’s rule not apply?

Answer 244

Goodsall’s rule does not apply to patients with Crohn’s disease

Question 245

Identification of anal fistula?

Answer 245

• Goodsall’s Rule

- Fibrous Tract: probing or fistulography under anesthesia

Question 246

What is a simple anal fistula?

Answer 246

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).

Question 247

What is a complex anal fistula?

Answer 247

Complex fistulas are higher along the gastrointestinal (GI) tract, have multiple tracts, involve other organs, are recurrent, or are associated with IBD or radiation.

Question 248

Are we more or less aggressive with cutting out the muscle when posterior anal canal is involved compared to the anterior anal canal.

Answer 248

Usually more aggressive cutting out muscle when posterior anal canal (especially in men), and less aggressive when anterior anal canal (especially in women)

Question 249

What is a fistulotomy?

Answer 249

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)

Question 250

Treatment of low lying fistula

Answer 250

Low lying fistula (does NOT involve external sphincter) > primary fistulotomy

Question 251

Treatment of high lying fistula

Answer 251

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)

Question 252

Treatment of complex anal fistula?

Answer 252

• 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

Question 253

Post-operative treatment of anal fistula?

Answer 253

Sitz bath, irrigation and packing to ensure healing from inside to outside (fistulas heal from the bottom up).

Question 254

Definition of pilonidal disease

Answer 254

Cyst/abscess near or on the intergluteal cleft of the sacrococcygeal area containing hair/skin debris

Question 255

Treatment of anal fistula

Answer 255

Surgery - Fistulotomy

Question 256

Epidemiology of pilonidal disease

Answer 256

Epi: usually young men age 15-35yr, rare in >50

Question 257

Pathophysiology of pilonidal disease

Answer 257

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

Question 258

Signs and symptoms of pilonidal disease

Answer 258

Asymptomatic or chronically itchy until acutely infected, then pain/tenderness, purulent discharge and increased moisture near the coccyx

Question 259

Treatment of pilonidal disease

Answer 259

• 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

Question 260

Signs and symptoms of proctalgia/levator ani syndrome

Answer 260

• 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).

Question 261

Indications of pilonidal disease?

Answer 261

Failure of healing after irrigation/debride, recurrent disease, or complex disease

Question 262

Most common tumor of anal canal

Answer 262

SSC of the anal canal

Question 263

Clinical features of SSC of the anal canal

Answer 263

Anal bleeding, pain, mass, ulceration, pruritus, 25% asymptomatic

Question 264

Treatment of SSC of the anal canal

Answer 264

Chemotherapy ± radiation ± surgery

Question 265

3 types of anal cancer?

Answer 265

• SSC of the Anal Canal
• Malignant Melanoma of Anal Canal
• Anal Margin CA

Question 266

Treatment of malignant melanoma of anal canal?

Answer 266

Wide excision or abdominal perineal resection ± chemoradiation

Question 267

Who should get a pap test of the anus/risk factors for anal cancer?

Answer 267

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

Question 268

Definition of chronic abdominal pain?

Answer 268

Pain that persists for more than 3 months either continuously or intermittently. Intermittent pain may be referred to as recurrent abdominal pain (RAP)

Question 269

Etiology of chronic abdominal pain?

Answer 269

1. 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
2. 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

Question 270

What should be asked on history for chronic abdominal pain?

Answer 270

• 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

Question 271

Physical exam for chronic abdominal pain?

Answer 271

• 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

Question 272

Red flags of chronic abdominal pain?

Answer 272

Fever, Anorexia, weight loss, Pain that awakens patient, Blood in stool or urine, Jaundice, Edema, Abdominal mass or organomegaly

Question 273

Investigations of chronic abdominal pain?

Answer 273

• 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.

Question 274

Ddx for dyspepsia?

Answer 274

• 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)

Question 275

Etiology of GERD?

Answer 275

• 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

Question 276

Definition of dyspepsia?

Answer 276

Chronic or recurrent epigastric pain, often with regurgitation, heartburn, bloating, nausea, and post prandial fullness (indigestion)

Question 277

Definition of heartburn?

Answer 277

Retrosternal burning sensation secondary to lower esophageal sphincter relaxation = more specific for GERD

Question 278

Approach to dyspepsia

Answer 278

• 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

Question 279

Investigations for dyspepsia

Answer 279

• 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

Question 280

Diagnosis of irritable bowel syndrome (IBS)?

Answer 280

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

Question 281

Symptoms of PUD

Answer 281

• 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

Question 282

Diagnosis of PUD?

Answer 282

• 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)

Question 283

Management of uncomplicated PUD?

Answer 283

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)

Question 284

Management of H. pylori-positive PUD?

Answer 284

• Classic triple therapy CLAMET:
  1. PPI (omeprazole) 20mg BID for 14 days
  2. clarithromycin 500mg BID
  3. Amoxicillin 1g BID and metronidazole

Question 285

Presentation/symptoms of IBD?

Answer 285

Both present with chronic diarrhea, possibly bloody, abdo cramping, urgency.

Question 286

Risk factors for IBD?

Answer 286

Age 15-40 y, jews, FHx of IBD, smoking (before for Crohn’s, after smoking cessation UC), western diet, NSAIDS

Question 287

Features of Crohn’s

Answer 287

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

Question 288

Complications of Crohn’s

Answer 288

Stricture, fistula, arthritis, irtis, episcleritis, erythema nodosum, pyoderma gangrenosum

Question 289

Diagnosis of Crohn’s

Answer 289

• Colonoscopy + intubation of ileum*
• Biopsy & histology confirm diagnosis
• Gastroscopy to assess UGI
• Small Bowel Assessment – MR/CT enterography – thickened colonic wall, wireless capsule endoscopy

Question 290

Symptoms of Crohn’s

Answer 290

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

Question 291

What does bx show for UC?

Answer 291

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

Question 292

Symptoms of UC?

Answer 292

Usually chronic bloody diarrhea, abdominal cramping, urgency, tenesmus, incontinence, mild fever, tachycardia, dehydration, anemia

Question 293

Diagnosis of UC?

Answer 293

• 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.

Question 294

Complications of UC?

Answer 294

Toxic megacolon (colonic distension >6cm + fever, anemia, HR >120, neutrophils >10.5, dehydration, hypotension, altered sensorium, electrolyte disturbance), perforation, stricture, colon cancer

Question 295

Features of UC?

Answer 295

Insidious onset, >4wks, chronic changes to mucosa→ mixed infiltrate, branched crypts, contiguous, mucosal disease, no granulomas.

Question 296

Treatment of IBD?

Answer 296

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).

Question 297

95% of diverticular disease occurs in

Answer 297

Sigmoid colon

Question 298

Risk factors of diverticulosis?

Answer 298

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)

Question 299

Symptoms and signs of diverticulosis?

Answer 299

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)

Question 300

Treatment of diverticulosis?

Answer 300

• 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

Question 301

Complications of diverticulosis?

Answer 301

Diverticulitis (15-25%), diverticulitis complicated with abscess/obstruction/perforation/fistula, bleeding (5-15% PAINLESS from rectum), diverticular colitis (rare: diarrhea, hematochezia, tenesmus, abdo pain)

Question 302

Pathophysiology of diverticulosis?

Answer 302

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

Question 303

Time period for acute viral hepatitis?

Answer 303

<6m

Question 304

Time period for chronic viral hepatitis?

Answer 304

> 6m

Question 305

Pathogenesis of viral hepatitis?

Answer 305

Virus infects hepatocytes creating MHC I proteins that are then attacked by CD8 T-cells for apoptosis leading to liver damage

Question 306

Symptoms of viral hepatitis?

Answer 306

• 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)

Question 307

Investigations/findings for viral hepatitis?

Answer 307

• 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

Question 308

Treatment for viral hepatitis?

Answer 308

• 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

Question 309

Defective RNA virus requiring HBsAg for entry into hepatocyte, therefore infects only patients with HBV?

Answer 309

Hepatitis D

Question 310

The presence of HBsAg indicates that the person is _____

Answer 310

Infectious

Question 311

The presence of anti-HBs would be found in?

Answer 311

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.

Question 312

In acute infection (<6 mos), anti-HBc is mainly of the ___ class, whereas in chronic infection, ___ anti-HBc predominates

Answer 312

IgM

IgG

Question 313

Antibody to HBcAg (anti-HBc, or HBcAb would be found in?

Answer 313

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.

Question 314

For hep B; ___ tends to suggest more active viral replication and greater infectivity. In contrast, presence of the corresponding antibody (____) suggests lower infectivity

Answer 314

HBeAg

anti-HBe

Question 315

Standard of care for hep C treatment?

Answer 315

Oral interferon-free regimens

Question 316

Mechanism by which acetaminophen induces damage on hepatocytes?

Answer 316

Mechanism: high acetaminophen dose saturates glucuronidation and sulfation elimination pathways - reactive metabolite is formed - covalently binds to hepatocyte membrane

Question 317

Presentation of acetaminophen induced liver disease?

Answer 317

• 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

Question 318

Treatment of acetaminophen induced liver disease?

Answer 318

• 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

Question 319

What is Wilson’s disease?

Answer 319

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

Question 320

Symptoms of Wilson’s disease?

Answer 320

• 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

Question 321

Screening test for Wilson’s disease?

Answer 321

1. reduced serum ceruloplasmin (<50% of normal)
2. Kayser-Fleischer rings (usually require slit-lamp examination)
3. increased urinary copper excretion (measure 24-hour urine copper)

Question 322

Gold standard for Wilson’s disease?

Answer 322

1. increased copper on liver biopsy by quantitative assay

2. genetic analysis imperfect as many mutations in ATP7B are possible

Question 323

Treatment for Wilson’s disease?

Answer 323

1. penicillamine chelates copper, poorly tolerated
2. trientine chelates copper
3. zinc impairs copper excretion in stool and decreases copper absorption from gut
4. tetrathiomolybdate preferred if neurological involvement

Question 324

What is hemochromatosis?

Answer 324

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)

Question 325

Etiology of primary (hereditary) hemochromatosis?

Answer 325

Hepcidin deficiency results in ongoing gut absorption of iron despite adequate iron stores

Question 326

Etiology of secondary hemochromatosis

Answer 326

• Parenteral iron overload (e.g. transfusions)
• Chronic hemolytic anemia: thalassemia, pyruvate kinase deficiency
• Excessive iron intake

Question 327

Clinical features of hemochromatosis

Answer 327

• 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

Question 328

Who should you screen and how to screen for hemochromatosis?

Answer 328

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

Question 329

Treatment of hemochromatosis?

Answer 329

• 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)

Question 330

Most common cause chronic liver failure

Answer 330

Alcoholic liver disease

Question 331

What are the three types of alcoholic liver disease

Answer 331

• Metabolic condition (fatty liver)
• Inflammatory condition (alcohol hepatitis)
• Fibrotic condition (cirrhosis)

Question 332

Clinical features of fatty liver

Answer 332

Mildly tender hepatomegaly; jaundice rare, mildly increased transaminases <5x normal

Question 333

Clinical features of mild alcohol hepatitis?

Answer 333

Mild: stops drinking because feels unwell, resumes when feeling better (if assessed, findings of hepatitis, potentially mild jaundice, and mildly elevated INR)

Question 334

Clinical features of severe alcohol hepatitis?

Answer 334

Severe: stops drinking but feels unwell, low grade fever, RUQ discomfort, increased white blood cell count - mimics RLL pneumonia and cholecystitis

Question 335

Investigations for alcoholic liver disease

Answer 335

• 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

Question 336

Treatment of alcoholic liver disease

Answer 336

• 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

Question 337

Risk factors of non-alcoholic steatohepatitis (NASH)?

Answer 337

DM, Male, hyperlipidemia, obesity

Question 338

Two types of non-alcoholic steatohepatitis (NASH)?

Answer 338

• 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).

Question 339

Presentation of non-alcoholic steatohepatitis (NASH)?

Answer 339

• Often asymptomatic
• May present with fatigue, malaise, and vague RUQ discomfort
• Elevated serum triglyceride/cholesterol levels and insulin resistance

Question 340

Investigations of non-alcoholic steatohepatitis (NASH)?

Answer 340

• Elevated serum AST, ALT ± ALP; AST/ALT <1

- Presents as echogenic liver texture on ultrasound

Question 341

Treatment of non-alcoholic steatohepatitis (NASH)?

Answer 341

• 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

Question 342

What is alpha-1-antitrypsin deficiency

Answer 342

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

Question 343

Two types of alpha-1-antitrypsin deficiency

Answer 343

• 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).

Question 344

Presentation of alpha-1-antitrypsin deficiency

Answer 344

Early emphysema, neonatal hepatitis syndrome, or cirrhosis carcinoma, elevated liver enzymes

Question 345

Diagnosis of alpha-1-antitrypsin deficiency

Answer 345

Serum A1AT level, Pi phenotype abnormal

Question 346

Treatment of alpha-1-antitrypsin deficiency

Answer 346

NONE for liver type – just treat complications, screen for carcinoma. If lung type, then can give A1AT infusion! Screen family.

Question 347

Definition of cirrhosis

Answer 347

Liver damage characterized by diffuse distortionofthebasicarchitecturewithfibrosisandformationof regenerative nodules

Question 348

Etiology of cirrhosis

Answer 348

• 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)

Question 349

Investigations of cirrhosis?

Answer 349

• 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

Question 350

Treatment of cirrhosis?

Answer 350

• 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

Question 351

Hematologic changes in cirrhosis

Answer 351

• Pancytopenia from hypersplenism: platelets first, then WBC, then hemoglobin
• decreased clotting factors resulting in elevated INR

Question 352

What is the strongest predictor of variceal development

Answer 352

Hepatic venous pressure gradient (HVPG) >10 mmHg

Question 353

Treatment of variceal bleeds?

Answer 353

Resuscitation, antibiotic prophylaxis, vasoactive drugs (e.g. octreotide IV) combined with endoscopic band ligation or sclerotherapy, Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Question 354

Classification of renal failure in cirrhosis?

Answer 354

• pre-renal (usually due to over-diuresis)
• acute tubular necrosis
• Hepatorenal Syndrome (HRS)

Question 355

What is type I hepatorenal syndrome (HRS)?

Answer 355

Type I: sudden and acute renal failure (rapid doubling of creatinine over 2 wk)

Question 356

What is type II hepatorenal syndrome (HRS)?

Answer 356

Type II: gradual increase in creatinine with worsening liver function (creatinine doubling over years)

Question 357

Hepatorenal syndrome (HRS) can occur at any time in severe liver disease, especially after:

Answer 357

• Overdiuresis or dehydration, such as diarrhea, vomiting, etc.
• GI bleed
• Sepsis

Question 358

Treatment of hepatorenal syndrome?

Answer 358

• For type I HRS: octreotide + midodrine + albumin (increases renal blood flow by increasing systemic vascular resistance)
• Definitive treatment is liver transplant

Question 359

Pathogenesis of hepatopulmonary syndrome?

Answer 359

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

Question 360

Clinical features of hepatopulmonary syndrome

Answer 360

• 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)

Question 361

Treatment of hepatopulmonary syndrome

Answer 361

Only proven treatment is liver transplantation

Question 362

Diagnosis of hepatopulmonary syndrome

Answer 362

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)

Question 363

Definition of portal hypertension

Answer 363

Pressure gradient between hepatic vein pressure and wedged hepatic vein pressure (corrected sinusoidal pressure) >5 mmHg

Question 364

Pathophysiology of portal HTN?

Answer 364

• 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)

Question 365

Signs of portal HTN?

Answer 365

Esophageal varices, Melena, Splenomegaly, Ascites, Hemorrhoids

Question 366

Complications of portal HTN?

Answer 366

• 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

Question 367

Treatment of portal HTN?

Answer 367

• Non-selective B-blockers (propanolol, nadolol, carvedilol) decrease risk of bleeding from varices
• TIPS: to decrease portal venous pressure

Question 368

Chronic stigmata of liver disease

Answer 368

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

Question 369

Definition of hepatic encephalopathy?

Answer 369

Spectrum of potentially reversible neuropsychiatric syndromes secondary to liver disease diagnosed after ruling out other causes for symptoms (e.g. structural/metabolic)

Question 370

Pathophysiology of hepatic encephalopathy?

Answer 370

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

Question 371

Precipitating factors of hepatic encephalopathy?

Answer 371

• 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

Question 372

Stages of hepatic encephalopathy?

Answer 372

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)

Question 373

What needs to be ruled out in order to diagnosis hepatic encephalopathy?

Answer 373

• 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)

Question 374

Treatment of hepatic encephalopathy?

Answer 374

• Lactulose: titrated to achieve 2-3 soft stools/d

- Oral rifaximin for both acute treatment and maintenance therapy has high level evidence for efficacy

Question 375

Why is lactulose used to treat hepatic encephalopathy?

Answer 375

• 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

Question 376

Definition of ascites?

Answer 376

Accumulation of excess fluid in the peritoneal cavity

Question 377

What should be calculated in order to determine the etiology of ascites

Answer 377

Serum [Alb] – Ascitic [Alb]

Question 378

Etiology of Serum [Alb] – Ascitic [Alb] >11 g/L (1.1 g/dL)

Answer 378

• Cirrhosis/severe hepatitis
• Chronic hepatic congestion
• Massive liver metastases
• Myxedema

Question 379

Etiology of Serum [Alb] – Ascitic [Alb] <11 g/L (1.1 g/dL)

Answer 379

• Peritoneal carcinomatosis
• TB
• Pancreatic disease
• Serositis
• Nephrotic syndrome

Question 380

Diagnosis of ascites

Answer 380

• Abdominal ultrasound
• Physical exam (clinically detectable when >500mL): bulging flanks, shifting dullness, fluid-wave test positive. Most sensitive symptom: ankle swelling

Question 381

Treatment of diuretic-sensitive ascites

Answer 381

• 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

Question 382

Treatment of refractory ascites

Answer 382

• Therapeutic paracentesis with intravenous albumin
• TIPS in anappropriate patient (no contraindications) with potential ltransplant-free survival advantage
• Liver transplantation

Question 383

Who should be on prophylaxis for spontaneous bacterial peritonitis (SBP)

Answer 383

• Cirrhosis or GI bleed: ceftriaxone IV daily or norfloxacin bid x7d
• Previous episode of SBP: long-term prophylaxis with daily norfloxacin or TMP-SMX

Question 384

Clinical features of spontaneous bacterial peritonitis (SBP)

Answer 384

• 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

Question 385

Diagnosis of spontaneous bacterial peritonitis (SBP)

Answer 385

• 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

Question 386

Treatment of spontaneous bacterial peritonitis (SBP)

Answer 386

• 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

Question 387

Etiology of vomiting and/or nausea?

Answer 387

• 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

Question 388

Causes of gastrointestinal system vomiting and/or nausea?

Answer 388

• 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

Question 389

Causes of CNS vomiting and/or nausea?

Answer 389

• 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

Question 390

What should be asked on history for vomiting and/or nausea?

Answer 390

• Onset of symptoms – abrupt or insidious
• Timing of symptoms
• Nature of matter
• Abdominal pain
• Associated symptoms/findings

Question 391

What could timing of symptoms tell you about vomiting and/or nausea?

Answer 391

• 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

Question 392

What could nature of matter tell you about vomiting and/or nausea?

Answer 392

• 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

Question 393

What could abdominal pain tell you about vomiting and/or nausea?

Answer 393

• 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

Question 394

What could associated symptoms/findings tell you about vomiting and/or nausea?

Answer 394

• 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

Question 395

Physical exam of vomiting and/or nausea?

Answer 395

• 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

Question 396

Investigations of vomiting and/or nausea?

Answer 396

• 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.

Question 397

What are the dopamine receptor blockers for the treatment of vomiting and/or nausea?

Answer 397

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)

Question 398

What are the prokinetic agents for the treatment of vomiting and/or nausea?

Answer 398

• 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).

Question 399

1st line treatment for the treatment of vomiting and/or nausea?

Answer 399

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

Question 400

What are the serotonin receptor blockers for the treatment of vomiting and/or nausea?

Answer 400

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.

Question 401

Signs and symptoms of jaundice?

Answer 401

• 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

Question 402

Etiology of unconjugated hyperbilirubinemia (pre-hepatic)?

Answer 402

• Overproduction (hemolysis, reabsorption of hematoma)
• Decreased hepatic uptake (congestive heart failure)
• Decreased bilirubin conjugation (Gilbert syndrome, neonatal jaundice)

Question 403

Investigations of jaundice?

Answer 403

• 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)

Question 404

Etiology of conjugated hyperbilirubinemia (hepatic)?

Answer 404

1. 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
2. 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
3. Hepatocellular injury
   - Common: Drugs, toxins, viral hepatitis
   - Less common: Alcohol-related liver disease, hemochromatosis, primary biliary cholangitis, primary sclerosing cholangitis, steatohepatitis, Wilson disease
4. Other (e.g., infiltrative states, fatty liver)

Question 405

Definition of primary biliary cholangitis (PBC)

Answer 405

Chronic inflammation and fibrous obliteration of intrahepatic bile ductules

Question 406

Etiology of primary biliary cholangitis (PBC)

Answer 406

Likely autoimmune (associated with Sjogren’s syndrome, scleroderma, CREST syndrome, rheumatoid arthritis (RA), thyroiditis)

Question 407

Epidemiology of primary biliary cholangitis (PBC)

Answer 407

Affects mainly middle-aged women (M:F=1:9)

Question 408

Signs and symptoms of primary biliary cholangitis (PBC)

Answer 408

• 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

Question 409

Investigations of primary biliary cholangitis (PBC)

Answer 409

• 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

Question 410

Treatment of primary biliary cholangitis (PBC)

Answer 410

• 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

Question 411

Definition of ascending cholangitis

Answer 411

Infection of the biliary tree

Question 412

Etiology of ascending cholangitis

Answer 412

• 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

Question 413

Signs and symptoms of ascending cholangitis

Answer 413

• Charcot’s triad: fever, RUQ pain, jaundice (50-70%)
• Reynolds’ pentad in patients with suppurative cholangitis: fever, RUQ pain, jaundice, hypotension, altered mental status

Question 414

Investigations of ascending cholangitis

Answer 414

• Increased WBC
• Usually increased ALP and bilirubin, ALT variably elevated
• Blood culture
• Abdominal U/S: CBD dilation, stones

Question 415

Treatment of ascending cholangitis

Answer 415

• 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)

Question 416

Definition of primary sclerosing cholangitis (PSC)

Answer 416

Chronic inflammation + fibrosis of bile ducts in response to portal bacteria in genetically predisposed, progresses to liver failure over 12 years

Question 417

What is idiopathic primary sclerosing cholangitis (PSC) often associated with?

Answer 417

Primary/idiopathic (most common) - associated with IBD, more commonly UC, in up to 70-80% of patients (usually male) with PSC

Question 418

Secondary causes of primary sclerosing cholangitis (PSC)

Answer 418

• long-termcholedocholithiasis
• cholangiocarcinoma
• surgical/traumatic injury (iatrogenic)
• contiguous inflammatory process
• post-ERCP
• associated with HIV/AIDS (“HIV cholangiopathy”)
• IgG4-related disease

Question 419

Signs and symptoms of primary sclerosing cholangitis (PSC)

Answer 419

• Often insidious, may present with fatigue and pruritus

- May present with signs of episodic bacterial cholangitis secondary to biliary obstruction

Question 420

Investigations of primary sclerosing cholangitis (PSC)

Answer 420

• 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

Question 421

Treatment of primary sclerosing cholangitis (PSC)

Answer 421

• 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

Question 422

What is Gilbert’s syndrome?

Answer 422

• Metabolic defect- failure of bilirubin conjugation (UDP transferase). Normal Hb, Normal liver enzymes. Benign, non-progressive, COMMON
• Isolated unconjugated hyperbilirubinemia

Question 423

Males or females more likely to get abdominal hernia?

Answer 423

M:F=9:1

Question 424

Risk factors for abdominal hernia?

Answer 424

• 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)

Question 425

Clinical features of abdominal hernia?

Answer 425

• 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

Question 426

Investigations for abdominal hernia?

Answer 426

• Physical examination usually sufficient
• U/S ¬ ± CT (CT required for obturator hernias, internal abdominal hernias, and Spigelian and/or femoral hernias in obese patients)

Question 427

What is defined as a reducible hernia?

Answer 427

When the contents can be replaced through the hernia defect. Repair is either deferred or done electively

Question 428

What is defined as a strangulated hernia?

Answer 428

Vascular supply of protruded viscus is compromised (ischemia). Requires emergency repair

Question 429

What is defined as an incarcerated hernia?

Answer 429

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

Question 430

Why do epigastric hernias develop?

Answer 430

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)

Question 431

Who are more likely to develop epigastric hernias

Answer 431

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)

Question 432

What causes an incisional hernia?

Answer 432

Results from poor wound healing in a previous surgical incision (infection, tension, malnutrition, intra-abdominal pressure, etc.) – occurs in 5-10% of abdo incisions

Question 433

What is a Littre’s hernia?

Answer 433

Hernia involving a Meckel’s diverticulum (Think alphabetically: Littre’s Meckel’s = LM)

Question 434

What is an spigelian hernia?

Answer 434

Hernia through the linea semilunaris (or spigelian fascia); also known as spontaneous lateral ventral hernia (Think: Spigelian = Semilunaris)

Question 435

What is a pantaloon hernia?

Answer 435

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)

Question 436

What is a Richter’s hernia?

Answer 436

Only part of bowel circumference (usually anti-mesenteric border) is incarcerated or strangulated so may not be obstructed

Question 437

What is a sliding hernia?

Answer 437

Part of wall of hernia sac formed by retroperitoneal structure (usually colon)

Question 438

What is diastasis of the rectus abdominis muscles (DRAM)?

Answer 438

Diastasis of the rectus abdominis muscles (DRAM) is characterised by thinning and widening of the linea alba

Question 439

Which types of hernias are more likely to strangulate?

Answer 439

Femoral&raquo_space; indirect inguinal > direct inguinal

Question 440

What are the indications for laparoscopic inguinal hernia repair?

Answer 440

1. Bilateral inguinal hernias
2. Recurring hernia
3. Need to resume full activity as soon as possible

Question 441

Treatment of abdominal hernia?

Answer 441

• 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

Question 442

Surgical technique for herniorrhaphy?

Answer 442

• 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

Question 443

Components of the spermatic cord

Answer 443

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

Question 444

Boundaries of Hesselbach’s triangle?

Answer 444

Inferior epigastric vessels, Inguinal ligament (Poupart’s), Lateral border of the rectus sheath. Floor consists of internal oblique and the transversus abdominis muscle

Question 445

Etiology of direct inguinal

Answer 445

Acquired weakness of transversalis fascia “Wear and tear”. Increased intra-abdominal pressure

Question 446

Anatomy of direct inguinal

Answer 446

Through Hesselbach’s triangle Medial to inferior epigastric artery Usually does not descend into scrotal sac

Question 447

Etiology of indirect inguinal

Answer 447

Congenital persistence of processus vaginalis in 20% of adults

Question 448

Most common hernia in men and women

Answer 448

Indirect inguinal

Question 449

Symptoms of indirect inguinal

Answer 449

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)

Question 450

Treatment of indirect inguinal

Answer 450

• 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

Question 451

Anatomy of indirect inguinal

Answer 451

Originates in deep inguinal ring Lateral to inferior epigastric artery Often descends into scrotal sac (or labia majora)

Question 452

Epidemiology femoral hernia?

Answer 452

Affects mostly females

Question 453

Etiology of femoral hernia?

Answer 453

Pregnancy – weakness of pelvic floor musculature. Increased intra-abdominal pressure

Question 454

Anatomy of femoral hernia?

Answer 454

• 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

Question 455

Treatment of femoral hernia?

Answer 455

SHOULD ALWAYS BE REPAIRED - McVay (Cooper’s ligament repair), mesh plug repair

Question 456

Two mechanisms of abdominal injuries

Answer 456

• Blunt: usually causes solid organ injury

- Penetrating: usually causes hollow organ injury or liver injury (most common)

Question 457

What are the views of FAST scan?

Answer 457

CARDIAC VIEW + LUQ VIEW + RUQ VIEW + PELVIC VIEW + ANTERIOR LUNG FIELD

Question 458

Most common organs to be injured in blunt trauma?

Answer 458

SPLEEN* > LIVER > MESENTARY > UROLOGIC > PANCREAS

Question 459

Two types of hemorrhage for blunt trauma?

Answer 459

Intra-abdominal and retroperitoneal

Question 460

Physical exam for blunt trauma

Answer 460

1. 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
2. Other systems to assess: cardiovascular, respiratory (possibility of diaphragm rupture), genitourinary, pelvis, back/neurological

Question 461

Investigations for blunt trauma

Answer 461

Labs: CBC, electrolytes, coagulation, cross and type, glucose, Cr, CK, lipase, amylase, liver enzymes, ABG, blood EtOH, B-hCG, U/A, toxicology screen

Question 462

Imaging is done for blunt trauma if?

Answer 462

• 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

Question 463

Management of blunt trauma?

Answer 463

• 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

Question 464

List the indications for a trauma laparotomy

Answer 464

• 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

Question 465

Indications for foley and NG tube in abdominal trauma?

Answer 465

Foley catheter: unconscious or patient with multiple injuries who cannot void spontaneously or is unconscious

Question 466

Indications for NG tube in abdominal trauma?

Answer 466

NG tube: used to decompress the stomach and proximal small bowel. Contraindicated if suspected facial or basal skull fractures

Question 467

Most common organs injured in penetrating trauma?

Answer 467

SMALL BOWEL > LIVER > COLON > STOMACH > DIAPHGRAM

Question 468

Management of penetrating trauma?

Answer 468

• General: ABCs, fluid resuscitation, and stabilization

- Gunshot wounds always require laparotomy

Question 469

Etiology of acute abdominal pain?

Answer 469

• 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

Question 470

GI disorder aetiologies for acute abdominal pain?

Answer 470

• Perforated viscus, bowel obstruction, ischemic bowel, appendicitis, strangulated hernia, IBD flare, esophageal rupture, peptic ulcer disease
• Diverticulitis, gastroenteritis, GERD, esophagitis, gastritis, IBS

Question 471

Hepatobiliary aetiologies for acute abdominal pain?

Answer 471

• Hepatic/splenic injury, pancreatitis, cholangitis, spontaneous bacterial peritonitis, Biliary colic, cholecystitis, hepatitis

Question 472

Genital aetiologies for acute abdominal pain?

Answer 472

Female: Ovarian torsion, PID, ectopic pregnancy, tubo-ovarian abscess, ovarian cyst, salpingitis, endometriosis

Male: Testicular torsion, epididymitis, prostatitis

Question 473

Red flags of acute abdominal pain?

Answer 473

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

Question 474

Imaging for acute abdominal pain?

Answer 474

• 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

Question 475

Labs for acute abdominal pain?

Answer 475

CBC, electrolytes, glucose, BUN/Cr, U/A ± liver enzymes, LFTs, amylase + lipase, B-hCG, ECG, troponins, VBG/lactate , INR/PTT, tox screen

Question 476

Classic triad of AAA?

Answer 476

1. acute abdominal or back pain 2. hypotension 3. pulsatile abdominal mass

Question 477

Indications for surgery repair of AAA?

Answer 477

Indications for surgery >6cm diameter, painful/tender on palpation, enlarging, distal emboli, thrombosis, obstruction/compression of adjacent viscera, rupture

Question 478

Diagnosis of AAA?

Answer 478

• 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.

Question 479

Treatment of AAA?

Answer 479

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.

Question 480

What is ectopic pregnancy?

Answer 480

Any pregnancy that is implanted outside of the endometrial lining in the uterine cavity. Most happen in the fallopian tubes

Question 481

Risk factors of ectopic pregnancy?

Answer 481

• 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

Question 482

Presentation of ectopic pregnancy?

Answer 482

Classic triad of amenorrhea, bleeding, and abdominal pain usually at 6-8wks.

Question 483

Signs and symptoms of pancreatitis?

Answer 483

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

Question 484

Common causes of pancreatitis?

Answer 484

• 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)

Question 485

Labs for pancreatitis?

Answer 485

CBC + Lytes + Urea + Creatinine + ALT/ALP + Total/Direct Bilirubin + Lipase (specific) + amylase

Question 486

Imaging for pancreatitis?

Answer 486

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)

Question 487

Complications of pancreatitis?

Answer 487

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

Question 488

What is a pseudocyst?

Answer 488

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

Question 489

Treatment options for pseudocyst?

Answer 489

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)

Question 490

Treatment of gallstone pancreatitis?

Answer 490

Cholecystectomy after inflammation has resolved but before discharge

Question 491

Management of pancreatitis?

Answer 491

• 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

Question 492

Treatment of necrotizing pancreatitis?

Answer 492

Step up approach of Percutaneous drain -> endoscopic transgastric drainage -> minimally invasive retroperitoneal necrosectomy

Question 493

Treatment of pancreas abscess?

Answer 493

Antibiotics and percutaneous drain placement or operative debridement and placement of drains

Question 494

Most common etiology of acute appendicitis in younger patients?

Answer 494

Lymphoid hyperplasia is thought to be common cause in younger patients

Question 495

Most common etiology of acute appendicitis in older patients?

Answer 495

Blockage by solid particles of stool fecaliths is more common etiology in adults

Question 496

Pathophysiology of acute appendicitis?

Answer 496

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

Question 497

Signs and symptoms of acute appendicitis?

Answer 497

• 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

Question 498

Ddx of acute appendicitis?

Answer 498

• 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

Question 499

Complication of acute appendicitis?

Answer 499

Appendiceal wall necrosis and translocation (gangrenous appendicitis) > Perforation and spillage of appendiceal contents > Peritonitis > Hemodynamic instability, sepsis, abdominal/appendiceal abscess

Question 500

What is a missed appendicitis?

Answer 500

When a patient does not seek care within 24h after developing appendicitis-like symptoms, a diagnosis of ‘missed appendicitis’ is provided

Question 501

Pathophysiology of missed appendicitis?

Answer 501

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

Question 502

Symptoms of missed appendicitis?

Answer 502

A few days of pain, sometimes 7-10 days. Some days may be worse than others

Question 503

Management of missed appendicitis?

Answer 503

• 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

Question 504

Indications for urgent appendectomy?

Answer 504

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)

Question 505

Prophylactic antibiotics to use for acute appendicitis?

Answer 505

Ideally, at least 60 minutes before surgery – ceftriaxone 2g daily, flagyl 500mg BID

Question 506

Investigations for acute appendicitis?

Answer 506

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

Question 507

Imaging for acute appendicitis?

Answer 507

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

Question 508

Functional/non-mechanical cause of bowel obstruction?

Answer 508

Ileus – impaired bowel motility. Common causes: opiates, electrolytes abnormalities (hypokalemia) or intra-abdominal infections

Question 509

Common mechanical SBO causes?

Answer 509

1. Intraluminal: intussusception, gallstones, Bezoars
2. Intramural: Crohn’s disease, radiation stricture, adenocarcinoma
3. Extramural: previous surgery adhesions (75% of SBO), incarcerated hernia, peritoneal carcinomatosis

Question 510

Symptoms & signs of SBO?

Answer 510

• 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

Question 511

Findings on AXR for SBO?

Answer 511

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

Question 512

Risk factors for SBO?

Answer 512

Prior abdominal surgery or presence of abdominal wall hernias

Question 513

Labs for SBO?

Answer 513

• 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

Question 514

Indications for emergency operation for SBO?

Answer 514

Peritonitis, high fever or high concern of ischemia, elevated white blood count, primary SBO (tumor) – all those that shouldn’t have adhesions

Question 515

Indications of surgery for SBO?

Answer 515

If no improvement or worsening sx after trial of conservative management then surgery is indicated. Complete obstruction, closed loop obstruction, perforation or dead gut

Question 516

Non-operative management of SBO?

Answer 516

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

Question 517

Complications of SBO?

Answer 517

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)

Question 518

Common mechanical LBO causes?

Answer 518

• Intraluminal: constipation, foreign bodies
• Intramural: adenocarcinoma, diverticulitis, IBD stricture, radiation stricture
• Extramural: volvulus, adhesions, hernias (sigmoid colon in inguinal groin hernia)

Question 519

Signs and symptoms of LBO?

Answer 519

Nausea/vomiting, colicky abdo pain, distention, constipation, bowel sounds normal/increased/absent if ileus

Question 520

Pathophysiology of open loop LBO?

Answer 520

Incompetent ileocecal valve allows relief of colon pressure as contents reflex INTO the ileum > clinical features are similar to SBO

Question 521

Pathophysiology of closed loop LBO?

Answer 521

Competent ileocecal valve results in proximal/distal occlusions and massive colonic distention then pressure in the cecum > bowel wall ischemia > necrosis > perforation

Question 522

What is functional/acute-pseudo obstruction?

Answer 522

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

Question 523

Findings on AXR for LBO?

Answer 523

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)

Question 524

Treatment of mechanical LBO?

Answer 524

Surgical correction of obstruction, usually resection and diverting colostomy – volvulus requires sigmoidoscopic/endoscopic decompression first, then if not, operative resection

Question 525

Treatment of functional LBO?

Answer 525

Treat underlying cause, NPO, nasogastric tube decompression (or rectal tube decompression, colonoscopy, neostigmine), or surgical decompression (ostomy/resection) uncommon

Question 526

What is paralytic ileus?

Answer 526

Temporary, reversible impairment of intestinal motility, most frequently caused by = abdominal operations, infections/inflammation, medications (opiates, anesthetics, psychotropics), electrolyte abnormalities

Question 527

Signs and symptoms of paralytic ileus?

Answer 527

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

Question 528

Investigations of paralytic ileus?

Answer 528

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

Question 529

Treatment of paralytic ileus?

Answer 529

NPO + fluid resuscitation + nasogastric decompression + correct causative abnormalities (e.g. sepsis, meds, electrolytes), consider TPN for prolonged ileus

Question 530

Etiology of intestinal ischemia?

Answer 530

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)

Question 531

Signs and symptoms of intestinal ischemia?

Answer 531

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

Question 532

Labs for intestinal ischemia?

Answer 532

Leukocytosis (nonspecific) + lactic acidosis (late finding) + get amylase/lactate/CK/ALP (observe progress) + hypercoagulability workup if suspect venous thrombosis

Question 533

Imaging findings of intestinal ischemia?

Answer 533

• 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

Question 534

Treatment of intestinal ischemia?

Answer 534

• 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

Question 535

Etiology of abdominal distension

Answer 535

1. Ascites
   - Portal HTN – Cirrhosis, Cardiac failure, Hepatic vein thrombosis
   - Normal Portal HTN - Cancer (especially ovarian), Pancreatitis, TB
2. Flatulence
   - Functional bowel disease (e.g. IBS)
   - Fibre
   - Lactose intolerance
   - Chewing gum (e.g. sorbitol, mannitol)
3. Feces
   - Constipation
   - Colonic obstruction
   - Dysmotility
4. Other
   - Pregnancy (fetus)
   - Obesity (fat)
   - Blood
   - Large tumours (fatal growth)

Question 536

Differential diagnosis of abdominal distention

Answer 536

6Fs: Fat, Feces, Fetus, Flatus, Fluid, Fetal Growth

Question 537

DDx of weight loss?

Answer 537

• 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

Question 538

Investigations of weight loss?

Answer 538

• 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