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Clinical Medicine 4 > Lecture 3 (GI)-Exam 1 > Flashcards

Lecture 3 (GI)-Exam 1 Flashcards

1
Q

Peptic Ulcer Disease
* Most commony where?
* May also occur where?

A
  • Most commonly in duodenal bulb (Duodenal Ulcer) & stomach (Gastric Ulcer)
  • May also occur in esophagus, pyloric channel, duodenal loop, jejunum
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2
Q

CONCEPT OF GASTRIC MUCOSAL BARRIER
* What is its role?
* What is the concept of cytoprotection?

A

Keeps integrity of luminal mucosa despite of a pH 1.

Concept of cytoprotection:
* Several mechanisms involved; integrity of mucosa and tight junctions. Mucous layer, including bicarbonate, protective prostaglandins, blood supply.

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3
Q
A
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4
Q

Peptic Ulcer Disease: Etiology
* Break in that what?
* What is the most common cause of the break? When was it discovered? How is it transmitted?

A

Break in the mucosa
* Helicobacter pylori (most common)- Spiral Urease-producing organism
* Discovered in 1983
* Transmission is fecal oral

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5
Q

Peptic Ulcer Disease: Etiology
* What is the 2nd MC cause? What are 4 others causes?

A
  • NSAIDs - #2 cause
  • Stress
  • Ethanol
  • Injury
  • Fewer than 1% are due to a gastrinoma (Zollinger-Ellison syndrome)
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6
Q

Peptic Ulcer Disease
* What are the complications? (5)

A
  • Bleeding
  • Perforation
  • Gastric Outlet Obstruction
  • Penetration causing acute pancreatitis
  • Intractability
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7
Q

Duodenal Ulcer
* What are the clinical features?
* What is the dx?

A

Clinical Features
* Burning epigastric pain 90” to 3 hr after meals, often nocturnal, relieved by food or antacids

Diagnosis
* Upper endoscopy (EGD) or UGI barium radiography-> need a biospy

Dude, give me food

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8
Q

UGI Duodenal Ulceration
* How does it appear on imaging?

A

Appears as an outpouch of contrast into ulcer base & surrounded by wall of ulcer.

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9
Q

Penetrating Acute Duodenal Ulcer Beyond Pylorus
* What will happen over time?
* What leads to pain?
* What does it mean to perforate? What does that lead to?

A
  • Ulcers will penetrate over time if they do not heal.
  • Penetration leads to pain
  • If ulcer penetrates through muscularis & through adventitia, then ulcer is said to “perforate” & leads to an acute abdomen.
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10
Q

Gastric Ulcer
* What are the clinical features?
* How do you dx?

A

Clinical Features
* Burning epigastric pain made worse by or unrelated to food
* Anorexia, food aversion, weight loss (40%)

Diagnosis
* Upper endoscopy with biopsy to exclude possibility that ulcer is malignant

Gee, I am not hungry

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11
Q

Endoscopic view of a Gastric Ulcer
* What does it show?
* What should all gastric ulcers undergo?

A
  • A yellow-based ulceration with a pigmented spot is visualized on gastric wall at transition between corpus & antrum
  • All Gastric Ulcers should be biopsied to RULE OUT a malignancy.
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12
Q

Different Tests for H. Pylori
* What are the different dx tests? (list them in terms of sensitivity)

A

Sensitivity goes down with each item
* Rapid urease test of antral biopsy (when endoscopy is required)
* Urea breath test
* Stool antigen testing for patients who are not taking PPIs or Bismuth and do not have acute GI bleeding
* Detection of antibodies in serum is least sensitive

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13
Q

Treatment Objectives in PUD
* What do you prescribe?
* Discont what?
* For Gastric Ulcers exclude what?

A
  • RX: Proton Pump Inhibitors
  • Discontinue NSAIDs!!!
  • For Gastric Ulcers exclude malignancy with a biopsy via endoscopy
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14
Q

Treatment Objectives in PUD
* All patients with a Gastric Ulcer should have a follow-up? Can reasonably assess H.pylori resolution after what?
* Eradicate what? Markedly reduces rate of what?

A

All patients with a Gastric Ulcer should have a follow-up endoscopy in 6-8 weeks to confirm healing
* Can reasonably assess H.pylori resolution after CAP therapy with urea breath test

Eradication of H. Pylori (if present)
* Markedly reduces rate of ulcer relapse & indicated for all Duodenal Ulcers and Gastric Ulcers associated with H. Pylori.

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15
Q

H. Pylori Erradication
* What is the first line therapy?

A

First-line Therapy (7–10 days) – triple therapy (CAP)
* Clarithromycin 500 mg twice daily +
* Amoxicillin 1 g twice daily +
* PPI standard dose twice daily (Omeprazole)

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16
Q

H. Pylori Erradication
* What is the second line therapy?

A

Second-line Therapy (10–14 days) – quadruple therapy
* PPI standard dose twice daily +
* Metronidazole 500 mg three times daily +
* Tetracycline 500 mg 4 times daily +
* Bismuth subcitrate 120 mg 4 times daily

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17
Q

Gastritis: Erosive
* What is it?
* Caused by what?
* May be what or associated with what symp?

A
  • Hemorrhagic gastritis, multiple gastric erosions
  • Caused by ETOH, NSAIDs, severe stress (burns, sepsis, trauma, surgery, shock, or respiratory, renal, or liver failure)
  • May be asymptomatic or associated with epigastric discomfort, nausea, hematemesis, or melena
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18
Q

Gastritis
* What type of dx?
* Atrophic; associated with what? (2)
* _ induced (2)

A
  • Is a pathology diagnosis. (cannot do visual-> get biopsy)
  • Atrophic; associated with H pylori, inducing an elevation of gastrin OR associated with reduction of intrinsic factor ->Pernicious anemia
  • Medication induced.
  • Irritant induced
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19
Q

Gastritis
* What is the txt?

A
  • Treatment; avoidance of irritants.
  • Eradication of H. pylori.
  • Use of PPI ‘s. and H2 blockers
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20
Q

Gastric Cancer
* Highest incidence of what?
* Twice as common in who?
* Almost never seen in who?

A
  • Highest incidence in Japan, China, Chile, Ireland
  • Twice as common in men as in women
  • Almost never seen in patients <40 y/o
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21
Q

Gastric Cancer
* What are the risk factors? (4)

A

Strong association with H Pylori

Increased incidence in lower socioeconomic groups

Dietary factors
* Nitrates
* Smoked foods
* Heavily salted foods

Genetic component suggested by increased incidence in first-degree relatives of affected

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22
Q
A
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23
Q

Pathology Gastric Cancer
* What is the mc type? Where does it occur?
* What are other types?

A

Adenocarcinoma in 85% - most common type
* 2/3 arising in antrum or lesser curvature

Other Types
* Lymphoma: Low grade tumor of mucosa-associated lymphoid tissue (MALT) or aggressive diffuse large cell lymphoma

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24
Q

What are the clinical features of gastric cancer? (6)

A
  • Progressive upper abdominal discomfort
  • Early satiety
  • Frequently weight loss, anorexia, nausea
  • Acute or chronic GI bleeding from mucosal ulceration
  • Dysphagia if location in cardia
  • Vomiting (pyloric involvement and widespread disease)

Red flag: I use to eat a lot but now not so much… Get EGD

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25
Q

Gastric cancer: PE findings
* Often what early on?
* What happens later? (3)
* What are the skin abnormalities?

A
  • Often unrevealing early in course
  • Later: abdominal tenderness, pallor & cachexia most common signs
  • Skin abnormalities (nodules, dermatomyositis, acanthosis nigricans (DM), or multiple seborrheic keratosis – lesser trelat sign)
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26
Q

Gastric cancer: PE findings
* Metastatic spread may be manifest by what?

A

Metastatic spread may be manifest by hepatomegaly, ascites, L SCL (Virchow’s node), periumbilical (Sister Mary Joseph’s node), ovarian (Kurkenberg Tumor), or prerectal mass (Blummer’s shelf)

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27
Q

Gastric Cancer
* What are the lab findings?
* How do you dx it?
* How do you stage it?

A
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28
Q

Gastric Adenocarcinoma
* What are the txt options?

A
  • Gastrectomy
  • Adjuvant +/- Neoadjuvant chemotherapy
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29
Q

Pyloric stenosis
* MCC of what?
* What are the causes?
* What is the sxs?

A
  • Most common cause of intestinal obstruction in infancy.
  • Causes: hypertrophy and hyperplasia of the muscular layers of the pylorus causes functional gastric outlet obstruction.
  • SXS – projectile vomiting
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30
Q

Pyloric Stenosis
* What are the PE findings?
* How do you dx it?

A
  • PE - A firm, non-tender, and mobile hard pylorus that is 1-2 cm in diameter, described as a mass “olive,” may be palpated in the right upper quadrant
  • DX – US (modality of choice) – hallmark is the thickened pyloric muscle
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31
Q

Pyloric Stenosis
* What is the txt? (2)

A
  • Correction of fluid loss with IV fluids
  • Corrective Surgery (long term control)
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32
Q

Rapid Gastric Emptying -> Dumping Syndrome
* What is it?
* What is the etiology?

A
  • Accelerated emptying of food boluses into the small intestines.
  • Etiology – peptic ulcer surgeries (Billroth I or II, Roux-en-Y, etc.)

Very common after gastric bypass Sx or peptic ulcer Sx or short gut type syndrome

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33
Q

Rapid Gastric Emptying -> Dumping Syndrome
* What are the sxs?
* What is the tx?

A
  • SXS - Epigastric fullness, pain, nausea, vomiting, early satiety, flushing, palpitations. Hypoglycemia symptoms from oversecretion of insulin
  • TX – small feedings of low-carbohydrate meals, separation of fluid and solid intake. (do not over power stomach)
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34
Q

Delayed gastric emptying
* What are the etiologies?
* What are the sxs?

A
  • Etiologies – there are many (idiopathic, medication induced, neurological), but Diabetic gastroparesis is the most important cause.
  • SXS – early satiety, bloating, gastric fullness, nausea. Symptoms are worsened by eating
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35
Q

Delayed Gastric Emptying
* What do you need to rule out??
* How do you evaluate it?

A
  • DDX: Need to rule out gastric outlet obstruction
  • Evaluation – Endoscopy may exclude a structural abnormality. UGI w/ small bowel follow through.
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36
Q

Delayed Gastric Emptying
* What is the tx?
* What can you prescribe?

A

TX – avoid meds that slow gastric emptying (anticholinergics, opiates, dopamine agonists, Tricyclic antidepressants). Avoid foods that are high in fat. Control DM.
* RX: Prokinetic medications – metoclopramide (Reglan) – long term SE is EPS.
* Botox and/or surgery

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37
Q

Gastric Outlet Obstruction
* What is the dx criteria? (2)

A
  • In a fasting patient (>8hours) upon 750ml saline bolus administration more than 400ml of liquids retained or aspirated with NG tube or upon EGD 30 minutes after ingestion.
  • Or of GI specialist is unable to reach duodenum during EGD
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38
Q

Gastric Outlet Obstruction
* What are the two types?
* What is the txt?

A
  • Benign vs malignant
  • Treatment: NG to intermittent suction. IV PPI ‘s. Reevaluation after 72 hrs
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39
Q

What is the normal anatomy of the pancreas?

A
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40
Q

Pancreatic Function
* What is the pancreatic function?

A

Islets of Langerhans secrete insulin & glucagon essential to regulation of glucose levels

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41
Q

Pancreatic Function
* What are the exocrine functions? (5)

A
  • Secrets a variety of digestive enzymes
  • Amylase: digests starches
  • Lipase: digests fats
  • Trypsin & Elastase: digest proteins
  • NaHCO3: serves to neutralize acidic contents of duodenum & jejunum to protect small intestinal epithelium
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42
Q

Pancreatitis
* What is it?
* Pancreatic inflammatory disease may be classified as what?
* Differentiation based on?

A
  • Inflammation and edema of acute pancreatitis resulting from inappropriate activation of pancreatic enzymes within the pancreas, with leakage of these enzymes into the interstitial space .
  • Pancreatic inflammatory disease may be classified as acute or chronic
  • Differentiation based on clinical criteria
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43
Q

Pancreatitis
* In acute pancreatitis, there is what?
* In chronic form there is what?

A
  • In acute pancreatitis, there is restoration of normal pancreatic function (high lipase +/- amylase and sxs of abdominal pain and vomiting)
  • In chronic form there is permanent loss of function & pain may predominate (progressive)
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44
Q

Acute pancreatitis:
* What is edematous pancreatitis? How do you treat it? (4)
* Necrotizing pancreatitis is more severe disorder in which what?

A

Edematous pancreatitis
* Usually mild & self-limited disorder
* Treat with lots of IV fluids (3rd spacing) and rest, NPO and pain management

Necrotizing pancreatitis
* More severe disorder in which degree of pancreatic necrosis correlates with severity of attack & systemic manifestations

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45
Q

Who gets pancreatitis? (13)

A
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46
Q

Acute pancreatitis-sxs
* Acute onset of what?
* Pain is what and where?
* What type of senstation?

A

Acute onset of abdominal pain, nausea, and vomiting.

Pain is steady, usually epigastric (occasional right or left upper quadrants of the abdomen)
* Also periumbilical.

“Boring” sensation that radiates into the back. (be careful because older folks-> think cardiac too)

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47
Q

Acute pancreatitis: sxs
* Often pain is worse and better when?
* Marked by what? What are the sxs? (5)

A
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48
Q

Acute pancreatitis: Physical exam findings
* Bowel soungs?
* Tenderness?
* Voluntary and rebound what?

A
  • Diminished or absent bowel sounds
  • Diffusely tender abdomen or focal tenderness in the epigastrium
  • Voluntary guarding, rebound tenderness
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49
Q

Acute Pancreatitis – Physical Exam Findings
* In less than one percent of cases: what are the signs?

A

Signs of hemorrhagic pancreatitis (Severe acute pancreatitis)
* Gray-Turner’s sign (flank ecchymosis)
* Cullen’s sign (periumbilical ecchymosis)

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50
Q

Acute pancreatisis
* you need two or more of what to dx acute pancreatits

A

2 or more of the following
1) characteristic abdominal pain
2) serum amylase and/or lipase ≥3 times the upper limit of normal
3) characteristic findings of acute pancreatitis on CT scan.

51
Q

Acute Pancreatitis Diagnosis
* What is the best imaging choice and why (4)

A

Abdominal CT is the best imaging choice
* Helpful if diagnosis is in question
* Helpful in determining prognosis
* Helpful in detecting complications
* US and CT are sensitive early because they show no changes

52
Q

Pancreatic Function Tests in Acute Pancreatitis
* Amylase: Abnormal rise when? Return to normal when?
* Lipase: rises when and how long?

A
53
Q

Acute Pancreatitis - Additional Tests
* What are additional tests? (6)

A
54
Q

Acute Pancreatitis Treatment
* What is the treatment?(5)

A
  • AGGRESSIVE IV fluid resuscitation
  • O2
  • Monitoring
  • Pain medications (Traditionally – use meperidine because does not cause contraction of the sphincter of Oddi)
  • Nutrition: NPO
55
Q

Acute Pancreatitis Treatment
* How should nurtrition work with txt?

A

nothing by mouth, then introduce oral nutrition when tolerating.
Patients who are unlikely to resume oral nutrition within 5 days because of sustained organ failure or other indications require nutritional support. Nutritional support can be provided by TPN or by enteral feeding. There appear to be some advantages to enteral feeding.

56
Q

Acute Biliary Pancreatitis - Treatment
* Patients with pancreatitis secondary to gallstones should receive a what?
* What is the txt if stone is distal?

A
57
Q

Acute Pancreatitis
* What is the prognosis?

A

85 to 90% of patients have self-limited course which resolves completely in 3 to 7 days after treatment is instituted

58
Q

the other ~10% that do not get better
* What happens in severe acute pancreatitis?
* What are local compliations? (4)

A

Severe Acute Pancreatitis: Acute pancreatitis with local and/or systemic complications

Local complications:
* Necrotizing pancreatitis
* Infected necrosis
* Pancreatic abscess
* Peripancreatic fluid collection and pseudocystic lesions

59
Q

the other ~10% that do not get better
* What are the systemic complications? (5)

A
  • Pulmonary and renal failure
  • Shock
  • Cardio-circulatory dysfunctions
  • Systemic sepsis
  • Coagulopathy
60
Q

Early Signs of Severe Acute Pancreatitis
* What are the signs? (7)
* What lab can be done?
* What score?

A
61
Q
A
62
Q

Chronic pancreatitis: etiology
* What is the most common cases?
* Obstuction of what?
* What other forms?
* _

A
  • Alcohol (most cases)
  • Duct obstruction
  • Hereditary or familial forms
  • Idiopathic
63
Q

Chronic pancreatitis: etiology
* What are the causes of Duct obstruction? (5)

A
  • Post-traumatic pancreatic duct strictures
  • Pancreas divisum: embryologic anomaly with impaired drainage of main pancreatic duct
  • Scarring or obstruction of pancreatic sphincters
  • Tumors: pancreatic cancer or tumor of ampulla
  • Cystic fibrosis
64
Q

Chronic Pancreatitis – Clinical Manifestations
* Chronic what?
* Symptomatic what? When does this occur?
* What can occur later on in disease?

A
  • Chronic abdominal pain, diarrhea, or weight loss.
  • Symptomatic malabsorption (steatorrhea) does not occur until pancreatic enzyme secretion is reduced to less than 10% of normal.
  • Diabetes mellitus may occur later in the disease. Patients are frequently insulin-dependent.
65
Q

Chronic Pancreatitis:
* What can be elevated or normal?
* What test is positive?
* What is the imaging studies and what does it should?

A
  • Amylase/lipase may be elevated or normal
  • Fecal elastase test is positive (low level) ✨
  • Imaging studies: KUB – pancreatic calcifications
66
Q

Chronic Pancreatitis: Tests to evaluate the etiology
* Abdomen US:
* CT scan:
* ERCP:

A
  • Abdomen US – may detect duct dilation, pseudocyst, calcification, and presence of ascites
  • CT scan – may detect calcifications, evaluate ductal dilation, and r/o pancreatic cancer
  • ERCP – evaluate presence of dilated ducts, strictures, pseudocysts, and intraductal stones
67
Q

Chronic Pancreatitis Treatment
* Avoid what?
* Meals?
* _ management
* Treat what? (2)

A
  • Avoid ETOH
  • Small, frequent, low-fat meals
  • Pain management
  • Treat steatorrhea with pancreatic supplements (i.e. pancrease, creon, pancrelipase)
  • Treat complications (i.e. DM)
68
Q

Pancreatic Pseudocyst
* What is it a major component of? Complication of?
* Sacs contain what?
* Typically found on what?
* What is the course of txt?

A
  • Make up 75% of all pancreatic masses and is a complication of acute pancreatitis
  • Sacs contain pancreatic enzymes, blood and necrotic tissue
  • Typically found on US or CT
  • Small cysts are observed, large one can be drained surgically
    * Endoscopy or CT-guided drainage
69
Q

Pancreatic cancer presentation
* What are non-specific sxs? (7)

A
  • “Painless jaundice” – Obstructive Jaundice by mass in pancreas
  • Vague crampy Abdominal pain
  • RUQ isnt painful upon palpation
  • Weight loss
  • Nausea
  • Systemic pruritis
  • Trousseau syndrome = Migratory thrombophlebitis assoc with malignancy
70
Q

Pancreatic cancer presentation
* How do you dx it?
* What is not reliable? why?

A
  • CT guided BX
  • Endoscopic Ultrasound (EUS) with biopsy
  • CA19-9 is not reliable because some patients with cancer don’t have elevated marker
    * Instead, use it to track response to therapy in those with elevated markers on chemo
71
Q

What are the most common site of pancreatic metastases?

A
72
Q

Pancreatic cancer txt:
* What surgery can be done? Who is this for?

A

Surgery
* Curative pancreatectomy (Whipple’s) – appropriate for only 10-20% of pts whose lesion is <5cm, solitary, and without METS. Adjuvant chemo may improve post-op survival
* Palliative surgery (for biliary decompression/diversion)

73
Q

Pancreatic Cancer Treatment
* Palliative therapeutic what?
* Chemo?
* What can be used for palliative care of pain?

A
  • Palliative therapeutic ERCP using stents
  • Chemotherapy – best combination chemotherapy in a patient with METS provides only a 19 week median survival
  • XRT for palliation of pain
74
Q

Inflammatory Bowel Disease (IBD)
* Peak onset?
* Second peak?
* Equal incidence btw who?
* Family?

A
  • Peak onset: 15-25 years of age
  • Second peak 50-65 years of age
  • Equal incidence between males and females
  • 10-15% occurrence in relatives
75
Q

Inflammatory Bowel Disease (IBD)
* What are enviromental triggers? (5)
* What is the pathophysiology?

A
  • Environmental triggers: Infections, Smoking (for Crohn’s), Stress, NSAIDs, Diet
  • Pathophysiology – Antigens trigger the immune response of IBD
76
Q

Under notes

Inflammatory bowel disease:
* Not what type of disorder?
* when pt comes in with flare-up, always check what?
* Smoking makes what worst? THey have what complications?
* What are other triggers?

A
  • The IBDs do have a peak onset around 15-25, then a second peak later in life. NOT an inherited disorder but there is some connection…
  • when pt comes in with flare-up, always do a check for INFECTION.
  • smoking makes Crohn’s disease worse. They’ll have a lot more complications—fistulas, abscesses. But interestingly, it’s protective against ulcerative colitis. (they’ve tried nicotine patches and the gum, but these are not effective)
  • other triggers: stress, NSAIDs, diet…but it’s an immune response that causes the problem
77
Q

What are the eye complication of IBD?

A
  • TONS of extraintestinal manifestations. Pt has bad diarrhea but also problems in other organs.
  • Ex: pt coming in with uveitis, (eye pain, photohobia, injection), could be presentation of IBD.
78
Q

What are the mouth complication of IBD?

A
79
Q

What are the complications of IBD with liver and gallbladder? (3) When should you suspect one of them?

A

Steatosis

Gallstones

Sclerosing Cholangitis
* Suspect in a patient w/ IBD who has unexplained elevated liver enzymes, particularly an elevation in serum alkaline phosphatase

80
Q

Under notes

Complications of IBD – Liver and Gallbladder
* Steatosis:
* Sclerosing cholangitis highly, HIGHLY associated with what? What does it cause? When to suspect this and dx how?

A

Steatosis – inflammation causes secretory type picture b/c electrolytes can’t be absorbed, pt not able to absorb things, could get malabsorption type picture.

Sclerosing cholangitis highly, HIGHLY associated with IBD—if you see a pt with this, should certainly get a colonoscopy to check for Crohn’s or UC.
* causes inflammation and scarring of intra and extrahepatic ducts. destroy the ducts, causing obstruction in liver; also the hepatic duct, cystic duct, CBD (outside liver).
* If pt just has an elevated alk-phos, suspect this. Dx with liver bx. If dx’d with scelorising cholangitis, then colonoscopy to look for IBD

81
Q

Other Complications of IBD
* What are other issues? (6)

A
82
Q

What are the skin complications of IBD?

A

Ex: pt comes in w/ this skin presentation. Looks like really bad infection.
* if threw ABX at this pt, wouldn’t help one bit.
* if sent for surgical debridement, would make it 10 x worse.
* this is PYODERMA, skin manifestation for IBD-> note the nice purple border which is Classic violaceous border that distinguishes it from others

83
Q

What is another complication of skin?

A
  • Very painful skin nodules.
  • SARCOIDOSIS pts also have this
84
Q
A
85
Q

Common laboratory findings in IBD
* What are the lab signs of inflammation? (3)

A
  • Leukocytosis
  • Elevated ESR (sedimentation rate)
  • Elevated CRP (c-reactive protein)

  • These pts can have elevated white count from their inflammatory state.
  • 2 inflammatory markers: SED RATE and CRP. They’re high in any inflammatory state, not very specific. But usually higher when pts have flares, are in acute state
86
Q

Common laboratory findings in IBD
* Some patients may have signs of what? How?
* What are the Signs of chronic blood loss?

A

Some patients may have signs of protein loss from the intestinal mucosa
* Low serum albumin

Signs of chronic blood loss
* Hypochromic, microcytic anemia (Iron deficiency anemia - low ferritin, elevated TIBC/transferrin, low serum iron)
* Occult blood in stool

If they’re losing chronic blood, can present with Fe deficiency anemia type picture.

87
Q
A

Crohn’s can affect anywhere from mouth to anus. Spotty involvement. Affects transmurally, so don’t usually present with bloody diarrhea b/c it affects entire layers, more often presents with fistula-type complications.

Ulcerative colitis affects only colon, rarely terminal ileum. Just the mucosa are involved here. mucosa gets very friable, this is why these pts present with rectal bleeding, BRBPR

88
Q
A

Crohn’s (fistula!)
* RLQ pain b/c iliocecal joint located there, and it’s the most commonly involved in Crohn’s disease. Pain and drainage in perianal area b/c of the fistula.
* ASCA can be + in Crohn’s pts.
* Smoking worsens this disease.

89
Q

Crohn’s Disease
* What are the three types?

A
  • Inflammatory
  • Obstructive
  • Fistulizing (enteroenteric, enterovesicular, enterocutaneous)
90
Q

Crohn’s Disease – Symptoms
* What are the sxs for inflam, obstructive, fistulizing?

A

Inflammatory
* Abdominal Pain, Tenderness, Diarrhea

Obstructive
* Abdominal Pain, Abdominal Distension, Vomiting,

Fistulizing (enteroenteric, enterovesicular, enterocutaneous)
* Diarrhea
* Pneumaturia

  • Can present with SB obstruction-type sxs…
  • Fistula can occur ANYWEHRE (enteroenteric = bowel on bowel; enterovesicular = on bladder; enterocutaenous = on skin). Air or feces in urine indicates enterovesicular fistula.
91
Q

What are the different locations for crohn’s disease? (5)

A
92
Q

How do you dx crohn’s disease? (4)

A
  • Clinical History
  • Exclude Infection
  • Appearance on Colonoscopy:Pathology (not during active flare phase-> tx with abx and steriods until flare is down then colonoscopy)
  • Serologic Testing
93
Q

Crohn’s Disease
* What are the distinguishing features? (8)

A
  • Granuloma
  • Skip Lesions
  • Asymmetrical involvement
  • Small Bowel involvement
  • Transmural involvement
  • Fistulas
  • Rectal Sparing
  • Bloody stools are not as common as in UC

Classic granuloma. Common imaging finding is SKIP LESIONS, STRING SIGN b/c it involves area, skips an area, another area, etc.
* transmural involvement, so ALL of the layers.
* this does spare the rectum, so typically don’t see rectal problems, but lots of perianal problems.

Can go from inflammatory to fistula-type problems

94
Q

What does this show?

A
95
Q

What does crohn’s disease look like in colonoscopy?

A

  • Do NOT do colonscopy when pt is having an active flare
  • Note “cobblestoning” and +- apthous ulcers
  • Transmural involvement.
96
Q

Serology – Crohn’s Disease
* What marker is positive?

A

ASCA – anti-Saccharomyces cerevisiae antibodies
* 61% sensitive, 88% specific for Crohn’s disease
* Most commonly seen in small bowel Crohn’s disease

Can test Ab for Crohn’s. not 100% sensitive and specific but can order if suspect it. Ultimately need colonoscopy with Bx

97
Q

What is a perianal complication of crohn’s disease?

A

Use seton to txt it

98
Q

Ulcerative Colitis
* What are the sxs? (5)

A
  • Bloody Diarrhea (small frequent bowel movements)
  • Urgency
  • Fever
  • Nocturnal Diarrhea
  • Improvement of symptoms with tobacco use

Friable appearancebloody diarrhea

99
Q

Ulcerative Colitis
* What is the location?

A

Location -> Limited to the COLON (with 1 exception)
* 40% distal colon
* 29% extensive pancolitis
* 30% proctitis
* ~1% in terminal ileum

If I remove this pt’s entire colon, it would cure their colitis.

100
Q

Ulcerative Colitis - Diagnosis
* How do you dx it?

A
  • Clinical History
  • Exclude Infection
  • Appearance on Colonoscopy->Pathology
  • Serologic Testing
101
Q

Ulcerative Colitis - Diagnosis
* What is shown on x-ray? What is this associated with?
* What is always involved?

A
  • Lead pipe showsloss of the normal haustral markings.
  • This ‘lead pipe’ appearance is associated with longstanding ulcerative colitis.
  • The distal bowel is always involved in this disease but, as there is no air in the descending colon, this segment of colon is not evidently abnormal.
102
Q

Serologic Testing - UC
* What is used for marker?

A

pANCA – perinuclear antineutrophil cytoplasmic antibodies
* 65% sensitive and 85% specific for Ulcerative Colitis

  • Blood test for ulcerative colitis.
  • Not specific for ulcerative colitis at ALL.
103
Q

What is a UC complication to the intestines?
* What do you need to get on these people?
* Ultimately sx, but want to control what?
* Can occur with what?
* A patient doing what?
* Normal what? Worry about hat?

A
  • Definitely do KUB on these pts
  • Ultimately sx, but want to control pt’s disease so they don’t end up in this state
  • Can occur with psuedomembranous colitis as well.
  • A pt not taking their meds can present with a flare.
  • note loss of normal HAUSTRA. Worry about RUPTURE.
104
Q

What is another UC complication of the intestines?

A

Both IBD have CA risk, but UC is much higher b/c it involves the colon.

105
Q

What is the Goals of IBD Treatment? (5)

A
  • Induce AND Maintain clinical remission
  • Improve patient’s quality of life
  • Heal mucosa
  • Decrease number of hospitalizations, surgeries.
  • Minimize therapy related complications

This really needs to be treated by GI physicians. Be aware of that. rule out infection and refer to GI.

106
Q

What medications do you need to give for IBD? (3)

A
107
Q

Medications in IBD
* The 5-ASAs target what? The rectal preps benefit the UC pts most b/c of what?
* Step up from that, pt with flare or new-onset presentation. Want to rule out what and how?
* Steroids VERY effective, but never want to do what?

A
  • The 5-ASAs target the immune response going on in the pt. the rectal preps benefit the UC pts most b/c of the rectal invovlement. We put pts with mild forms of IBD on these.
  • Step up from that, pt with flare or new-onset presentation. Want to rule out infection, so labs on stool… then ABX, commonly used together for GI: metronidazole and Cipro to put pts in remission. Check w/GI doc
  • Steroids VERY effective, but never want to put pt on them yourself, always under GI physician, because once started, hard to get pt off of it.
108
Q

Corticosteroid use in IBD
* induces what?
* What are the SE? (6)

A
109
Q

Medications in IBD
* What are the immunomodulator drugs?

A

Immunomodulator Drugs
* Azathioprine (Imuran)
* Cyclosporine
* Methotrexate

These immunomodulator drugs are a lot more toxic to pts but a lot more effective than 5-ASAs—reserved for really severe pts

110
Q

Medications in IBD
* What are the biologic therapies? What do need? Very effective in what? What type of concern?

A
  • Biologic Therapies (work against TNF – alpha)
  • Infliximab (Remicade)
  • Adalimumab (Humira)
  • Need PPD before consider these drugs b/c really suppress immune system
  • Very effective in preventing fistulas in Crohn’s
  • Lymphoma concern
111
Q

IBD – Indications for surgery
* What is the surgery and what are the UC indications (6)?

A

Panproctocoletomy
* Failure of or intolerance to medical therapy
* Dysplasia or Carcinoma
* Debility/Poor quality of life
* Massive hemorrhage
* Bowel perforation
* Intractable pyoderma

112
Q

IBD – Indications for surgery
* What is the surgery and what are the crohn’s disease indications (6)?

A

Surgery should be directed to specific complication
Symptomatic Obstruction
* Symptomatic Fistulae
* Bowel Perforation
* Massive Hemorrhage
* Dysplasia or Carcinoma
* Perianal Disease

113
Q
A
114
Q

What do you see pathology with crohns and UC?

A
115
Q
A
116
Q

Irritable Bowel Syndrome
* Altered what?
* What type of hypersensitivity?
* Impact of which neurotransmitter? How? (4)

A
117
Q

under slides

Irritable Bowel Syndrome
* Sort of dx of what? Has to do with what? Pts are what?
* something to do with what?
* What is predominant?

A

NOT to be confused with IBD
* sort of a Dx of exclusion. Has to do with altered bowel motility. Pts are hypersensitive, so abdominal pain is a predominant symptom.
* something to do with serotonin, so drugs have tried to target that…
* diarrhea or constipation predominance or combination of 2

118
Q

IBS sxs:
* Abdominal pain and discomfort with what? (3)
* Abdominal what?
* What is in the stool?

A

Abdominal pain/discomfort with
* Diarrhea Predominance
* Constipation Predominance
* Alternating Diarrhea with Constipation

Abdominal Bloating

Mucous in the stool

119
Q

IBS - Symptoms
* _ urgency
* Feeling of what?
* What are the associated GI sxs?
* What are other sxs?
* high link to what?

A
  • Fecal Urgency
  • Feeling of incomplete stool evacuation
  • Associated GI symptoms – difficulty swallowing,
  • Other Symptoms – headache, insomnia, myalgias, TMJ disorder, back/pelvic pain
  • 50% of fibromyalgia patients have IBS
120
Q
A
121
Q

IBS:
* How do you dx it?

A

Diagnosis of exclusion – rule out other causes of constipation/diarrhea – CBC, ESR, CMP, stool studies, TSH, colonoscopy to differentiate from IBD

122
Q

What are the red flags (malignancy) of IBS? (7)

A
  • Age >50
  • Unexplained weight loss
  • Iron deficiency anemia
  • Evidence of GI bleeding
  • Persistent or progressive pain
  • Family history of Colon Cancer
  • Fasting diarrhea >300ml/day
123
Q

Treatment of IBS
* Reassurance and supportive what?
* For diarrhea, use what?
* What is FDA approved for consitpation IBS?
* What other things might be effective?

A
  • Reassurance and supportive patient relationship, avoidance of stress or precipitating factors
  • For diarrhea, trials of Loperamide, Lomotil (diphenoxylate/atropine), or cholestyramine
  • Linaclotide (Linzess)… FDA approved for constipation IBS
  • Psyllium, fiber, certain antispasmodics, and peppermint oil may be effective
124
Q

Treatment of IBS
* Evidence suggests that some probiotics may be effective in what?
* What may relieve pain?
* What do you use for severe refractory cases?

A
  • Evidence suggests that some probiotics may be effective in reducing overall IBS symptoms but more data is needed
  • Amitriptyline 25-50 mg PO QHS or other antidepressant in low doses may relieve pain
  • Psychotherapy of benefit in severe refractory cases

Clinical Medicine 4 (15 decks)

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