MLS Exam 3: GI disorders/UTI/stones

Gastroesophageal reflux disease (GERD)

Reflux of stomach contents into the esophagus and occasionally up to the throat/mouth

what are etiologies/exacerbating factors of GERD?

LES dysfunction/incompetence

Hiatal Hernia

Irritant effects of refluxate

Decreased esophageal clearance of acid

Delayed gastric emptying

what is a common complication of GERD?

reflux esophagitis

what are the typical symptoms of GERD?

Pyrosis

Regurgitation

Dyspeptic symptoms

what is the PE like in a patient with ONLY GERD?

normal

the severity of symptoms of GERD correlates with the severity of disease t/f

false

1 multiple choice option

name some "extraesophageal" symptoms of GERD

Chronic cough

Vocal hoarseness/laryngitis

Sore throat

Globus sensation

Exacerbations of asthma/COPD

Atypical/non-cardiac chest pain

Sinusitis

Dental decay

what are red flag symptoms of GERD?

Dysphagia

Odynophagia

Weight loss

Frequent N & V

Epigastric or non-cardiac chest pain

Early satiety

Iron deficiency anemia

GI bleeding

what do red flag symptoms indicate the need for?

additional testing & work-up in conjunction with empiric medication management

most patients DONT need testing for GERD. you can start treatment without it. what is this called?

empiric therapy

what are diagnostic study options for GERD?

Esophagogastroduodenoscopy(EGD) +/- bx

Barium Upper GI series

24-hour esophageal pH monitor +/- manometry

when would you a barium upper GI series?

For patients with dysphagia

what is a 24-hour esophageal pH monitor +/- manometry indicated for?

patients with persistent symptoms despite BID PPI therapy or pre-surgery

when could you NOT initiated therapy based on history for GERD?

if there are red flag symptoms

what are lifestyle modifications that can help with GERD?

Small frequent meals

Weight loss

Avoid lying down, bending, heavy lifting & tight clothes after meals

Elevate the head of the bed (HOB)

Avoid drugs that decrease LES tone

what are antacids used for?

rapid relief of occasional heartburn

what do H2 blockers do and which is the most potent?

Block stimulation of acid secretion by binding to histamine receptors in the stomach

famotidine (Pepcid®)

what do proton pump inhibitors do?

Covalently bonds to the H+/K+-ATPase enzyme & inactivates it permanently

which inhibits acid secretion better? H2 blockers or PPIs

PPIs

1 multiple choice option

what are DDIs with PPIs?

Interferes with absorption of drugs that require acidic environments - Increase absorption of digoxin (Lanoxin®)

Omeprazole (Prilosec®) also has specific DDIs due to CYP450 interference

what DDIs does Omeprazole (Prilosec®) have?

prolongs metabolism & elimination of of diazepam (Valium®), warfarin (Coumadin®), and phenytoin (Dilantin®)

Speeds up metabolism & elimination of clopidogrel (Plavix®)

what are long term issues associated with using PPIs?

Decrease Ca2+, Fe, Mg2+ & B12 absorption

Increased risk of infectious gastroenteritis

Elevated serum gastrin levels

Gastric atrophy/polyp formation

what is a serious complication of GERD?

Barrett's esophagus (adenocarcinoma)

a complication of GERD is esophageal stricture. what are symptoms of this?

Gradual progression of solid-food dysphagia over months to years

May see DECREASED heartburn as stricture worsens & other symptoms progress

how do you diagnosis esophageal stricture? what is used initially and what is confirmatory?

Barium UGI (initially)

EGD with biopsy (confirmatory)

Barrett Esophagus/Esophagitis

Squamous epithelium replaced by metaplastic columnar epithelium

what confirms diagnosis of barrett esophagus/esophagitis?

EGD with biopsy

what is the worst complication of barrett esophagus?

adenocarcinoma (esophageal cancer)

how do you screen for esophageal cancer?

EGD w/biopsy every 3-5 yrs

what are the treatment options for barrett esophagus?

Proton pump inhibitor (PPI) therapy QD/BID

Ablative therapy

what are indications in which you would do ablative therapy?

Pts with Barrett’s + dysplasia

what is the procedure called for antireflex surgery?

Nissen fundoplication

Helicobacter pylori

Gram-negative rod that resides in antrum of stomach

H. pylori secretes many factors that compromise integrity of gastric/duodenal mucosa. name 1 example.

urease

Human host mounts an additional inflammatory response to H. pylori, further damaging epithelium causing what?

Gastritis, ulcer formation

describe the incidence and prevalence of H. pylori disease in the US

Rare in childhood, incidence increases with age

Present in ~100% of patients by age 70

how is H. pylori transmitted?

oral-oral

fecal-oral

H. pylori is almost always associated with what?

chronic active gastritis

H. pylori accounts for majority of?

PUD cases

what can H. pylori infection lead to and what does it also play a role in?

B12 malabsorption & anemia; MALT lymphoma & gastric CA

what are all the ways to test for a H.pylori infection?

Serology – IgM, IgA, IgG*

Urea breath test (UBT, [BreathTek®])*

Fecal H. pylori antigen testing (FAgT)*

Rapid urease testing (RUT, [CLOTest®, PyloriTek®])*

Bacterial culture (again, EGD sample)

what is an important consideration in regards to testing for H.pylori?

Must be off PPI x 7-14 d & ABX 28 d before test

what is gastritis and how is it histologically documented?

Inflammation (-itis) of the gastric mucosa

EGD biposy

what are the 3 categories of gastritis?

1. Erosive/Hemorrhagic*

2. Non-Erosive/Non-Hemorrhagic*

3. Histologically-specific gastritis

Erosive/Hemorrhagic

acute gastropathy

Non-Erosive/Non-Hemorrhagic

chronic gastropathy

Acute Erosive/Hemorrhagic Gastritis is related to local irritants/pathology like?

NSAIDs/ASA, Alcohol, toxins, caustic ingestion, portal hypertension/varices (end result of chronic liver disease), etc.

stress gastritis falls into the acute erosive/hemorrhagic gastritis category due to severe?

medical or surgical illness

EGD findings of acute erosive/hemorrhagic gastritis include?

Hemorrhages, petechiae, erosions

Usually superficial epithelial damage only

Very little true inflammation, if any

what is the cause of chronic gastritis type A?

autoimmune

what is inhibited/the problem in chronic gastritis type A?

Antibodies to parietal cells and

H+/K+-ATPase enzyme pump inhibited

why is having antibodies to parietal cells bad?

Parietal cells make intrinsic factor

Associated with pernicious anemia

what can the inhbition of H+/K+-ATPase enzyme pump lead to?

hypo- or achlorhydria with a subsequent ↑ in gastrin secretion (feedback loop)

patients with chronic gastritis type A are at ↑ risk for what?

gastric malignancy

what parts of the stomach is chronic gastritis type A mainly in?

fundus and body

what is the cause of chronic gastritis type B?

H. pylori

Location of chronic gastritis type B depends on predisposing genetic factors. what are the types of disease and which one do majority of patients have?

diffuse mild gastritis (majoirty)

antral predominant disease

body prominent disease

chronic gastritis type B can also increase the risk/lead to what?

gastric malignancy

how do you diagnosis chronic gastritis?

UPPER ENDOSCOPY (EGD) with tissue biopsy

what is an ulcer?

Break in gastric or duodenal mucosa

Occur when normal mucosal integrity and defensive factors are impaired or overwhelmed

what is the depth typically in a peptic ulcer?

through the muscularis mucosa down to the submucosa

how big usually are peptic ulcers?

>5 mm

what the 2 locations for peptic ulcers?

stomach and duodenum

stomach ulcers are typically located where?

antrum

what are more common stomach or duodenal ulcers?

duodenal

1 multiple choice option

what are more risk for malignancy, stomach or duodenal ulcers?

stomach

1 multiple choice option

what are peptic ulcers caused by and what is the leading cause?

Helicobacter pylori infection (leading cause)

NSAID-induced injury

how does gastric acid play a role in peptic ulcers?

DOES NOT play a role in PRIMARY ulcer development

BUT DOES contribute to CONTINUED mucosal injury once the insult has taken place

in NSAID-Induced PUD, severity of symptoms does NOT correlate with pathology t/f

true

1 multiple choice option

what do NSAIDs do?

inhibit cyclooxygenase (COX 1, COX 2 or both) and ↓ prostaglandin (PG) synthesis

what are symptoms of PUD?

Burning epigastric pain with changes related to meals

“Gnawing”

Ill-defined aching sensation

Hunger pain (“pangs”)

Duodenal Ulcer Symptoms

Pain usually occurs 90 min to 3 hours after a meal and is frequently relieved by food or antacids

2/3 will describe pain awakening them from sleep between midnight and 3 A.M.

Gastric Ulcer Symptoms

May be different than duodenal ulcer symptoms

Discomfort may actually be precipitated by food

Nausea & anorexia occur more commonly in gastric ulcer patients

name 3 complications of PUD

bleeding, perforation, gastric outlet obstruction

what is the most common complication of PUD? the least?

most: bleeding

least: gastric outlet obstruction

how does bleeding as a result of PUD present?

hematemesis or melena

penetration

a type of perforation in which the ulcer bed tunnels into an adjacent organ

what is the most common finding on PE in PUD?

Epigastric tenderness

what is the procedure of choice when diagnosing PUD?

endoscopy (EGD)

what are treatment options for gastritis and PUD?

Address underlying cause & heal mucosa

Medication

Surgery

Acid suppression therapy

Mucosal repair therapy

H. pylori eradication

name 3 types of acid suppression therapy

1. Antacids

2. H2 receptor antagonists/blockers (H2RA/H2B)

3. Proton pump (H+ K+ ATPase) inhibitors (PPI)

what are antacids used more for?

symptomatic relief of dyspepsia

how long should a patient be on H2RA/H2B for duodenal and gastric ulcers?

6 weeks for duodenal & 8 weeks for gastric

PPIs

Preferred(?) over H2B for treatment of ulcers

4-6 weeks for duodenal & 8 weeks for gastric

what are 3 things involved in mucosal repair therapy?

1. Cytoprotective Agents - Sucralfate (Carafate®)

2. Bismuth containing preparations

3. Prostaglandin Analogues

what is the most common side effect of cytoprotective agents and how do they work?

constipation; Binds to proteins within the ulcer bed and forms a barrier

Bismuth containing preparations are often used in the treatment of?

H. pylori

what are prostaglandin analogues used to prevent and what are 2 side effects?

used to prevent NSAID-induced ulcers; Diarrhea and

Uterine bleeding & contractions

all PUD patients who are (+) for H. pylori are getting H. Pylori eradication therapy that consists of?

Quadruple therapy and treat x 14 days

gerneral approach to therapy

(1) Document presence of ulcer or gastritis via EGD

(2) Is patient (+) for H. pylori?

No - Acid-suppression therapy

Yes - QT regimen x 14 d + continued acid suppression

(3) Is ulcer likely NSAID-related?

(4) Document Healing - Another scope (EGD)

what are refractory ulcers?

Gastric ulcer that fails to heal by 12 weeks

Duodenal ulcer that fails to heal after 8 weeks

why is document healing with another scope important?

Check for other problem (i.e. Zollinger-Ellison Syndrome [ZES], cancer, etc.)

what are options for surgical therapy for PUD?

Vagotomy

Pyloroplasty

Antrectomy

Zollinger-Ellison syndrome (ZES)

Rare condition characterized by gastrinoma (NET) with hypersecretion of HCl & recurrent ulcers

60% of gastrinomas are ______

malignant

diagnosis of ZES

Draw fasting gastrin level If elevated, get imaging to look for tumor:

Somatostatin receptor scintigraphy (SRS)

what is the best treatment for ZES?

High dose PPI therapy

etiology/pathophysiology of cholelithiasis

Bile stored in gallbladder becomes supersaturated

Particles precipitate out, form microscopic crystals

Crystals grow, aggregate, & fuse to form stone(s)

etiology/pathophysiology of acute cholecystits

Stone moves & obstructs cystic duct which leads to distention, inflammation, and potential secondary infection of the gallbladder

with acute cholecystitis, you can also have acalculous cholecystitis which is?

Sludge and/or biliary dyskinesia