Digestive pathophysiological Flashcards
(218 cards)
1
Q
Difference between NAFLD, NASH and NAFL
A
NAFLD: fatty liver disease spectrum
NAFL: Simple steatosis
NASH: Steatosis + inflammation + injury
2
Q
Cirrhosis w/o any obvious etiologies
A
Cryptogenic cirrhosis
3
Q
Epidemiology of NAFLD
A
Men > women
Hispanics > whites
Whites > blacks
4
Q
Polymorphism associated with NAFLD and what does it encode
A
PNPLA3 → encodes adiponutrin
5
Q
Most important risk factor for NAFLD
A
Insulin resistance
6
Q
Percentage of px with metabolic syndrome that have NAFLD
A
80%
7
Q
Role of insulin resistance to the progression of NAFLD
A
Increases lipolysis in adipose tissue → elevated free fatty acids in bloodstream → taken by liver and re-esterified into triglycerides → hepatic steatosis → excessive FFA cause oxidative stress → inflammatory pathway activation → chronic inflammation triggers stellate cells → fibrosis
8
Q
How do free fatty acids create liver injury and fibrosis
A
Chronic inflammation and injury → activation hepatic stellate cells → fibrosis
They potentiate lipid peroxidation and release of hydroxyl free radicals
9
Q
Hormone produced by omental fat in adipose tissues
A
Adiponectine (ACRP30)
10
Q
Levels of adiponectine that predispose to NASH progression
A
Low levels
11
Q
Symptoms and signs of NAFLD
A
Abnormal serum aminotransferase levels
Usually asymptomatic
12
Q
Maximum alcohol consumption for it to be considered NAFLD
A
2 standard drinks per day for men and one standard drink per day for women (70 g alcohol)
13
Q
Lab findings in NAFLD
A
Modest elevation ALT and AST 2-3x upper limit
AST/ALT ratio <1.0
14
Q
Mainstay imaging study for NAFLD and its finding
A
Ultrasonography → diffuse echogenic pattern in setting of hepatic fat accumulation
15
Q
Imaging study to evaluate degree of fibrosis in liver
A
Ultrasound based technique of VCTE
16
Q
Histological findings of NAFLD
A
Hepatocellular steatosis
Balloon degeneration
Mixed inflammatory cell infiltrates
Necrosis
Glycogen nuclei
Mallory hyaline
17
Q
Cornerstone of therapy for NAFLD
A
Improve insulin resistance through weight loss
18
Q
How do antidiabetic agents reduce insulin resistance
A
Activates nuclear hormone receptor PPARy → increase insulin sensitivity by enhancing adiponectin production in subcutaneous and visceral fat
19
Q
Harmful alcohol consumption
A
+ 4 drink/day or +14 drink/week for men
+3 drinks/day or +7 drinks/week for women
20
Q
Main risk factor for alcoholic fatty liver disease
A
Excessive alcohol consumption
21
Q
Maximum dose of acetaminophen with alcohol consumption
A
2 g
22
Q
Enzymes in charge of metabolizing alcohol and what do they produce
A
Alcohol dehydrogenase (ADH) and microsomal ethanol oxidizing system (MEOS)
They convert alcohol to acetaldehyde
23
Q
Why is acetaldehyde highly toxic
A
It cann bind to various macromolecules and activate immune response by activating DAMPs
24
Q
CYP in charge of microsomal oxidation
A
CYP2E1
25
Most common manifestation of alcoholic fatty liver disease
Steatosis
26
Complication of alcoholic fatty liver disease due to persistence drinking
Cirrhosis
27
Engorged veins in abdominal wall arranged either in palisade pattern or centered at umbilicus
Caput Medusae
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Lab findings of alcoholic fatty liver disease
Elevations of AST/ALT at 2:1 ratio
29
Predominant anemia in alcoholic liver disease
Macrocytic anemia
30
What does the Child-Turcotte-Pugh score evaluate
Albumin
Bilirubin
Prothrombin time
Ascites
Hepatic encephalopathy
31
What does the end-stage liver disease (MELD) score evaluate
Bilirubin
Prothrombin time
Creatinine
32
Main therapeutic approach for alcoholic liver disease
Management of alcohol consumption
33
Main pharmacological drugs for alcohol consumption
Disulfiram: acetaldehyde dehydrogenase inhibitor
Naltrexone: opioid receptor antagonist
Acamprosate: N-methyl-D-aspartate receptor antagonist
34
Only pharmacological drug for alcoholic liver disease that is not metabolized in liver
Acamprosate
35
Pharmacological therapy for variceal bleeding, ascites and hepatic encephalopathy
Non selective B-blockers → variceal bleeding
Loop diuretics and aldosterone antagonists → ascites
Lactulose → hepatic encephalopathy
36
Acute illness that typically develops in response to consumption of large amounts of alcohol (>120 g/day) for considerable amount of time
Alcohol associated hepatitis
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Most widely used prognostic marker for alcohol liver disease
Maddrey discrimination function (MDF)
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Prognostic marker that assesses response to corticosteroids
Lille
39
Cornerstone of medical tx for severe alcohol associated hepatitis
Corticosteroids
40
Requirement for liver transplantation in alcohol liver disease
6 month abstinence from alcohol
41
Hepatitis virus that produce and do not produce chronic infection
No: Hepatitis A and E
Yes: Hepatitis B, C, D
42
Transmission of hepatitis A
Fecal-oral
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Incubation and viremia period of hepatitis A
Incubation period → 2-6 weeks
Duration of viremia → 5-7 days
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Pathogenesis of hepatitis A virus
Liver damage due to host immune cell-mediated cytotoxicity
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Complication of hepatitis A
Cholestatic phase
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Clinical findings of hepatitis A
Podromal symptoms
Jaundice, dark urine and pale stools
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% of patients who are symptomatic and asymptomatic with hepatitis A infection
70% adults symptomatic
70% children asymptomatic
48
Antibodies that indicate an active hepatitis A infection
Anti-HAV IgM antibodies or HAV RNA
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Antibodies that indicate immunity due to prior infection or vaccination of hepatitis A infection
Anti-HAV IgG antibodies in absence of anti-HAV IgM antibodies
50
Mode of transmission of hepatitis B
Sexual, parenteral, vertical
51
Four open reading frames that encode 4 major proteins in hepatitis B
S gene → codes HBsAg
C gene → codes HBcAg and HBeAg
Pol gene → codes DNA polymerase
X gene → codes X protein
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Primary marker of HBV infection
HBsAg
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Population more prone to chronic infection of hepatitis B
Neonates (>90%)
54
Hepatitis B variants
Precore mutations → HBeAg negative chronic infection
S mutation → infants born to HBV-infected mothers but acquire HBV infection after vaccination
P mutation → resistance to antiviral agents lamivudine, adefovir, telbivudine
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Incubation period of acute hepatitis B
4 weeks to 6 months
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Clinical findings of acute hepatitis B
Aminotransferase elevations
Serum-sickness like syndrome
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Complication in children of acute hepatitis B
Papular acrodermatitis of childhood
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Antibodies detected in chronic hepatitis B
Persistence HBsAg
Detectable HBeAg
Anti-HBc is IgG class
59
Pathological findings in acute and chronic hepatitis B
Acute hepatitis → Councilman bodies (eosinophilic single-cell necrosis)
Chronic hepatitis → Ground glass appearance
60
1st line therapy for hepatitis B and its function
Entecavir → inhibits HBV polymerase, reverse transcription of negative HBV DNA, and synthesis of positive HBV DNA
Tenofovir disoproxil fumarate → inhibits reverse transcription RNA to DNA
61
Leading cause of chronic liver disease
Hepatitis C
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Recommendations for hepatitis C prevention
Recommended universal one-time screening for all >18 years old
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Clinical features of hepatitis C
Same clinical features as hepatitis B but milder and progression to chronicity is more common
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Histology of hepatitis C
Dense lymphocytic portal inflammatory infiltrate and hepatocellular steatosis
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How are ALT values in hepatitis C
ALT values fluctuate in saw-tooth type pattern
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Antibodies for active and resolved hepatitis C infection
Active infection: HCV RNA and Anti-HCV antibodies
Resolved infection: Anti-HCV antibodies
67
What is the sustained virologic response
Absence HCV RNA in serum 12 weeks following completion of antiviral therapy
68
Pharmacotherapy for hepatitis C
Sofosbuvir (NS5B inhibitor) and Velpatasvir (NS5A inhibitor) for 12 weeks
OR
Glecaprevir (NS3/4 protease inhibitor) and pribentasvir (NS5A inhibitor) for 8 weeks
69
Pathophysiological characteristic of hepatitis D
HDV requires HBV infection to complete virion assembly → uses HBsAg
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Histological findings in acute hepatitis D
Microvesicular steatosis
Granular eosinophilic necrosis
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Unusual form of delta hepatitis where superinfection can result in acute liver failure, with jaundice, fever and black vomit
Labrea fever
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Only licensed drug for HDV
PEG-IFN-a
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Transmission of hepatitis E virus
Fecal-oral
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4 major genotypes of hepatitis E
1 and 2 → common in endemic areas, virulent, severe cases
3 and 4 → in non endemic areas, nonvirulent and associated with inapparent infection
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Incubation period of hepatitis E
2-10 weeks
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Clinical features of hepatitis E
Similar to acute hepatitis A but more severe
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Risk population for hepatitis E
Pregnant women
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Treatment of drug induced liver injury
Remove drug
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Most frequent cause of drug induced liver injury
Acetaminophen
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Drugs commonly involved in drug induced liver injury
Acetaminophen
Amoxicillin-clavulanate
Isoniazid
Statins
Herbal agents and dietary supplements
81
Definition of diarrhea
As a symptom → increase in frequency, volume and often urgency of passage of stool and as a decrease in stool consistency
As a sign → having begun within 14 days of presentation
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Classification of diarrhea
Osmotic diarrhea: improves with fasting, due to Celiacs, pancreatic insufficiency, lactuose intolerance, osmotic laxatives
Secretory diarrhea: does not improve with fasting, due to stimulant laxatives or hormone-related
Inflammatory diarrhea: causes bloody diarrhea, due to IBD or infections (Shigella, EHEC, Campylobacter)
Acute non inflammmatory: watery diarrhea due to viral infections, ETEC, Staph aureus, V cholerae, etc
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Maximum absorptive capacity of small intestine and colon
Small intestine: 12 L
Colon: 4-6 L
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Major mechanisms of diarrhea
Enhanced mucosal secretion
Impaired epithelial absorptive and digestive activity
Increased permeability of epithelial barrier
Decreased absorptive surface
Altered motility
Increased intraluminal osmolarity
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Nonabsorbable laxatives associated with diarrhea
Magnesium citrate or magnesium hydroxide
Polyethylene glycol 3350
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Classification of diarrhea based on duration
Acute → <14 days
Persistent → 15-30 days
Chronic → >30 days
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Site of involvement of diarrhea based on characteristics
Large volume with little urgency, no tenesmus, moderate increase in stool numbers → small intestine and proximal colon
Frequent, low-volume dysenteric stools with blood and mucus associated with urgency and tenesmus → rectum and distal colon
88
In what type of diarrhea are fecal leukocytes present and what do they indicate
Dysenteric stools → indicates inflammatory colitis or enterocolitis
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Bloody diarrhea + absent leukocytes, what would it suggest
Amebiasis
90
Main organisms where fecal leukocytes are usually present
Shigellosis
Campylobacter
Invasive E coli (EIEC)
91
Main organisms where fecal leukocytes are usually absent
Norovirus
Rotavirus
V cholerae
Enterotoxic E coli (ETEC)
Enterohemorrhagic E coli
Staph or Bacillus cereus
Giardiasis
Amebiasis
92
Indications to do a stool examination for ova and parasites
When diarrhea persists +2 weeks
History of travel
Exposure children to daycare
History of immunosuppression or IBD
Homosexuals
Unexplained peripheral eosinophils
93
Gold standard to evaluate C difficile toxin
Cytotoxicity assay during cultured fibroblasts
94
Recommended approach to evaluate C difficile toxin
Screening with GDH (clostridial glutamate dehydrogenase) or PCR and then specific test with EIA for toxin A and B
95
What would be a low stool osmotic gap and what would you interpret from it
<50 mmol/L
Secretory diarrhea → high secretion or inhibition of water absorption
Functional diarrhea → increased intestinal movement
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What would be a high stool osmotic gap and what would you interpret from it
>100 mmol/L
Osmotic diarrhea → osmotic pull of ingested substances draws water into intestinal lumen
97
Gram (-) bacilli that is a major cause of dysentery infectious colitis
Shigella
98
Shigella: Acid labile or acid resistant?
Acid resistant
99
Mechanism of action of Shigella
S dysenteriae produces Shiga toxin
100
Type of diarrhea produced by Shigella
Watery diarrhea that progresses to dysenteric stools with mucus and blood
101
Severe complication of S dysenteriae
HUS → microangiopathic anemia, thrombocytopenia, acute renal failure
102
Gram (-) bacili that is found in contaminated water supplies
Vibrio cholerae
103
Mechanism of action of V cholerae
Cholera toxin over activates adenylate cyclase → increased levels AMPc → loss of chloride, sodium and water from intestinal epithelial cells
104
V cholerae: acid sensitive or acid resistant?
Acid sensitive
105
Type of diarrhea found in V cholerae
Watery diarrhea
106
Vaccines available for V cholearae
rBS-WC vaccine → oral vaccine with toxin B → V cholera O1 and ETEC
Bivalent vaccine → V cholera O1 and O139
107
Gram (-) bacili that is B-hemolytic
E coli
108
E coli variants that cause bloody diarrhea
Enterohemorrhagic (EHEC)
Enteroinvasive (EIEC)
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Most common cause traveler's diarrhea
Enterotoxigenic (ETEC)
110
Virulence factors of ETEC
Heat labile toxin (LT) → resembles cholera toxin; stimulates cyclic adenosine monophosphate production
Heat stable toxin (STa) → stimulates cyclic guanosine monophosphate production → enhanced chloride and water secretion and impaired Na chloride absorption
111
E coli that causes disease in infants and <2 years old
Enteropathogenic (EPEC)
112
Virulence factors of EPEC
Attaches to brush-border surface of enterocytes → activates pathways that alter cytoskeletal components → effacement of absorptive surface, increased epithelial permeability and altered epithelial barrier function
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Virulence factors of EAEC
Autoagglutination in stacked arrangement → mediated by aggregative adherence fimbriae I (AAF1)
Inflammation
114
E coli associated with chronic diarrhea and growth retardation
Enteroaggregative (EAEC)
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E coli with similar clinical features and virulence factors as Shigella
Enteroinvasive (EIEC)
116
Most common serotype of EHEC
O157:H7
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Virulence factors of EHEC
Produces Shiga-like toxin (Stx-1 and 2) → inhibits 60S ribosomal subunit
causes mechanical hemolysis
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Complication of EHEC
HUS
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Chronic disorder resulting from low retrograde flow of gastroduodenal contents into esophagus
Gastroesophageal reflux disease (GERD)
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Main pathophysiological mechanism of GERD
Transient inappropriate relaxation of LES
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Normal function of the lower esophageal sphincter (LES)
Chronically contracts to maintain pressure above 15 mmHg of intragastric pressure
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Gastric factors that promote GERD
↑ gastric volume after meals
↑ gastric pressure due to obesity
Recumbency after meals
Delayed gastric emptying
Gastroparesis
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Medications that decrease LES pressure (4)
B adrenergic agonists
A adrenergic antagonists
Anticholinergics
Calcium channel blockers
124
Foods that exacerbate GERD symptoms (6)
Caffeine
Chocolate
Peppermint
Alcohol
Citrus fruits
Carbonated beverages
125
Lifestyle factors that exacerbate GERD symptoms
Weight gain
Smoking
Eating prior to recumbency
126
Typical clinical features of GERD
Heartburn, regurgitation, dysphagia
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Alarm signs for GERD (7)
Dysphagia
Odynophagia
Weight loss
Family history GI tract cancers
Persistent nausea/emesis
Long duration symptoms (>10 years)
Incomplete response tx
128
Duration of symptoms where you would consider GERD
Typical symptoms >2 days/week for >4-8 weeks
129
Atypical manifestation associated with GERD
Asthma (30-80% px)
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Regurgitated gastric contents reach upper aerodigestive tract and what is their clinical picture
Laryngopharyngeal reflux → cough, hoarseness, sore throat, globus, otitis media
131
Classic GERD diagnosis
Thorough symptoms history and confirmed by complete response to medical therapy
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When is diagnosing testing required
Dx testing for those who fail PPI trial or have alarm signs
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Radiologic studies for GERD and their function
Barium swallow and upper GI series
To rule out other conditions or assess complications
134
Function of upper endoscopy in GERD
Exclude other diseases and detect grade/severity of GERD esophagitis
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Initial test of choice for complicated GERD px or refractory symptoms to therapy
Upper endoscopy
136
When would you do an esophageal biopsy in GERD
When eosinophilic esophagitis is suspected
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Acid exposure time values
AET >6% → conclusive evidence GERD
AET 4-6% → borderline or inconclusive
AET <4% → evidence against GERD
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Total reflux episodes values
Total reflux episodes <40 → evidence against GERD
Total reflux episodes >80 → adjunctive evidence of GERD
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Complications of GERD
Esophageal ulcers
Peptic esophageal strictures
Esophageal carcinoma
140
Cornerstone of treatment for GERD
Lifestyle modifications
141
Examples of lifestyle modifications for GERD (6)
Avoid foods and acid-containing beverages that can exacerbate symptoms
Avoid lying down for 3 hrs after eating
Smaller and frequent meals
Elevation of head of bed by 6 inches
Avoid wearing tight-fitting clothing
Stop smoking and lose weight
142
Function of antacids in GERD
Symptom relief by neutralizing refluxed acid gastric (increases esophageal pH)
143
Function of PPIs
Block hydrogen-potassium ATPase on apical surface parietal cells
144
Initial therapy of px with moderate-severe GERD and px with complications of GERD
PPI therapy
145
Complications of PPI therapy
Reduction on vitamin B12 levels
Higher rates community acquired pneumonia, C difficile, hip fractures
146
Mainstay of reflux therapy
Surgery
147
Most used surgical procedure for GERD and what does it do
Nissen fundoplication → wraps fundus around bottom of esophagus to enhance antireflux barrier
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Treatment for GERD px with obesity
Bariatric surgery
149
Management of peptic strictures
Esophageal dilations and PPIs
150
Characteristic to start medication withdrawal in GERD
Symptoms relief should be sustained 2-3 months
151
Complication of prolonged blockade PPIs
Rebound hypersecretion
152
Replacement of normal squamous epithelium of distal esophagus with specialized intestinal metaplasia
Barrett esophagus
153
Risk factors for progession to adenocarcinoma from Barrett
Dysplasia
Long segment Barrett
Mucosal abnormalities: nodules, ulcerations, strictures
154
Main cause of Barrett esophagus
Chronic GERD
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Epidemiology of Barrett esophagus
Males
Caucasians
Middle-aged
156
Risk factors for Barrett esophagus
Smoking
Drinking
157
Pathogenesis of Barrett esophagus
Increased levels refluxed acid concentrations → acid and bile induce Cdx genes → metaplasia
158
Gold standard dx for Barrett esophagus
Upper endoscopy with biopsy of distal esophagus
159
IMPORTANT
Barrett dx defined as presence of 3 cm columnar-lined distal esophagus with SIM
160
Criteria that determines extent of disease for Barrett
Prague criteria
161
Indications for screening for Barrett esophagus
For px over 50 with chronic GERD symptoms
162
Treatment for non dysplastic Barrett
Once daily PPI
163
A biopsy obtained adjacent to ulcer presents numerous neutrophils infiltrate epithelium; type of Barrett?
Indenitive dysplasia
164
Management of indefinite dysplasia Barrett
Aggressive PPI therapy and repeat surveillance biopsies in 3 months
165
Management of low grade dysplasia
Repeat EGD with surveillance biopsies within 3-6 months to confirm it is highest grade lesions
166
Management of high grade dysplasia
Endoscopic therapy
167
True or false: high grade dysplasia must be confirmed by a GI pathologist
FALSE: It must be confirmed by two different GI pathologists
168
How are surveillance biopsies for high grade dysplasia Barrett
Every 1 cm in all 4 quadrants of barrett segments as well as any suspicious nodules/ulcerations to rule out malignancy
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Mucosal defects in stomach or small intestine
Peptic ulcers
170
Most common causes of peptic ulcer disease
H pylori infection, NSAIDs, aspirin
171
Complications of peptic ulcer disease
GI bleeding, perforation, obstruction
172
Diagnosis of peptic ulcer disease
Endoscopy
173
Pathophysiology of peptic ulcer disease
Imbalance protective and aggressive factors such as when GI mucosal defense mechanisms are impaired in presence of gastric acid and pepsin
174
Risk factor that promotes development of ulcers
Smoking
175
Population where idiopathic ulcers are more common
Elderly with comorbidities
176
Spiral gram (-) urease-producing bacteria
H pylori
177
How does H pylori survive the acid environment of the stomach
Ability to produce urease → helps alkalize acid pH
178
Malignancies associated with H pylori infection
Gastric adenocarcinoma and MALT lymphoma
179
Carcinogen classification of H pylori
Group 1 carcinogen
180
Virulence factors of H pylori that facilitate attachment of bacteria to gastric epithelium
BabA and OipA
181
How does CagA promote H pylori infection and damage
Encodes type IV secretion island that elicits IL-8 production → affects cell growth and cytokine production
182
How do NSAIDs promote peptic ulceration
Inhibition COX1 → impairs mucosal protection and leads to ulcers
183
Classic symptom of peptic ulcer disease
Epigastric pain → gnawing, dull, aching, empty sensation
184
Clinical differences between duodenal and gastric ulcers
Duodenal → relieved with ingestion of milk, food, antacids but recurs 2-4 hrs after eating
Gastric → eating exacerbates pain, nausea and anorexia, relief when fasting
185
Definitive diagnosis for peptic ulcer disease
Upper endoscopy and biopsy
186
Ulcers more likely to be malignant
Ulcers >3 cm in size and those associated with mass
187
Px with multiple ulcers, refractory ulcers or ulcers in unusual locations, or who have diarrhea and weight loss
Zollinger-Edison syndrome
188
Limitation of barium studies in peptic ulcer disease
Do not permit biopsy to examine for histologic evaluation
189
Why shouldn´t serologic testing be used to determine success of cure after H pylori treatment
Antibody titers can persist for years and are not always negative
190
Initial diagnostic and follow up eradication therapy testing for H pylori infection
Urease breath test or stool antigen test
191
192
Characteristics for the urea breath test or stool antigent test for H pylori
Urea breath test → detect H-pylori derived urease activity in stomach
Stool antigen test → use polyclonal anti-H pylori capture antibody absorbed in microwells
193
Indication for testing H pylori successful cure
Wait at least 4 weeks after completing eradication therapy to confirm successful cure
194
Histologic testing for H pylori
Presence polymorphonuclear leukocytes in inflamed gastric tissue in biopsy
195
Most common complication of peptic ulcer disease
GI hemorrhage
196
True or false: ALL ulcers should be tested and treated for H pylori
TRUE
197
Risk assessment tool for peptic ulcer disease
Glasgow-Blatchford score
198
Indications for px with chronic NSAID use that cannot take it out
Consider taking lowest effective dose along with co therapy with PPI or misoprostol
199
Indications for aspirin use in peptic ulcer disease
Aspirin should be restarted as soon as risk for cardiovascular events outweighs risk for recurrent ulcer complications
200
General characteristics of H pylori treatment
PPI combined with 2+ antibiotics for 7-14 days
201
When should clarithromycin, metronidazole or levofloxacin be avoided in H pylori treatment
In areas where resistance rates are >15% → resistant to treatment
202
1st line therapy for H pylori infection
Bismuth quadruple therapy
PPI 2x daily + 4x daily tetracycline and metronidazole + bismuth
203
1st line therapy in areas with low primary resistance to clarithromycin
Concomitant therapy
2x daily PPI, amoxicillin, metronidazole, clarithromycin
204
Indications after failure of 2nd attempt of H pylori treatment
Consider culture with susceptibility testing
205
H pylori gastric carcinogenesis
Chronic gastritis → atrophy → intestinal metaplasia → dysplasia → adenocarcinoma
206
Prevalence of GERD in general population
10-20%
207
How does a hiatal hernia cause GERD
The negative pressure of the torax produces reflux
208
Prevalence of Barrett to cancer transformation
0.5%
209
Diagnostic test for patients with suspected H pylori on PPI use
Stool antigen testing
210
Treatment for H pylori in pregnant women
H2 receptor antagonists or antacids
211
Most likely ulcer to lead to perforation
Anterior duodenal ulcer
212
Extraintestinal manifestation of gastric ulcer perforation
Left shoulder pain
213
Type of ulcer related to patients in the ICU and their treatment when there is a high risk of bleeding
Stress related ulcer
You give PPI and enteral feeding
214
Los Angeles classification for GERD
A: <5 mm
B: >5 mm
C: <75% circumference
D: >75% circumference
215
Prevalence of GERD patients with Barrett
12%
216
Score to assess risk of hepatitis to advance to fibrosis
Fib-4
217
Component of the alcohol metabolism that produces steatosis
NADH
218
Lile score to continue the use of corticosteroids and to stop using them in alcohol associated hepatitis
Lile >0-45: stop use
Lile <0.45: continue use
