Dilate with Bougie Prevent recurrence (often time same cause as esophagitis)

Epigastrum Flashcards by Stephanie Marks

GERD: what to ask pt about

Relaxation of LES:
•Alcohol, tobacco, spicy foods, caffeine, chocolate

Obesity
Hiatal hernia
Pregnancy

Decreased saliva
•Tobacco, Sjogren’s

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GERD possible progression (5)

Gastroesophageal Reflux Disease (GERD)
•Passage of gastric contents into the esophagus

Reflux esophagitis
•Inflammation of the esophagus secondary to reflux

Esophageal stricture
•Scaring of the esophagus secondary to long standing reflux

Barrett’s esophagus
•Replacement of squamous epithelial cells with columnar cells due to GERD

Esophageal Adenocarcinoma

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GERD alarm features

New onset symptoms > 60 years old
New iron deficiency anemia
Dysphagia
Odynophagia
Weight loss
Evidence of bleeding (hematemesis, melena)

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How do you reach a GERD diagnosis?

•Based off clinical history and physical exam*
–In the setting of acute chest pain, GERD is a diagnosis of exclusion

•Symptoms improve with empiric treatment (PPI, H2B)

•Ambulatory 24-48h pH monitoring
–Reserved for GERD diagnosis in question or refractory GERD symptoms

•Endoscopy
–Especially for Alarm Features

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GERD treatment

1.Lifestyle modifications
–Decrease EtOH, caffeine, spicy foods, chocolate consumption
–Eat smaller, low-fat meals
–Weight reduction
–Smoking cessation
–Incline head of bed at night

2.Acid suppression with PPI
–Typically, a 2-month duration then taper
–PPI is only recommended for erosive esophagitis
–H2B can assist with GERD symptoms only

3.Surgery–Hiatal hernia repair

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Esophagitis treatment

Treat underlying cause (infectious, GERD, EoE)
PPI therapy
Sucralfate? Local anesthetic?

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Stricture treatment

Dilate with Bougie
Prevent recurrence (often time same cause as esophagitis)

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PUD symptoms

•Epigastric pain
–May radiate to the left and right upper quadrants
–Duodenal ulcers: hours after eating, pain awakening the patient from sleep
–Gastric ulcers: during or minutes after eating

Bloating
Early satiety
Nausea and/or vomiting
Bleeding –Hematemesis, hematochezia, melena

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Gastroparesis symptoms

Symptomatic delayed gastric emptying in the absence of mechanical obstruction

Nausea (90%)
Vomiting (70-80%)
Abdominal pain (rarely predominant symptom)
Early satiety
Bloating

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PUD Risk factors

•NSAIDS
•H Pylori
•Tobacco use
•COPD
•CKD
•CAD

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Gastroparesis Risk Factors

•Diabetes mellitus
•Medications– esp. Opioids
•Viral (CMV, EBV, VZV, Norwalk, rotavirus)
•Post-Surgical
•Scleroderma
•Paraneoplastic dysmotility–Dang Small Cell Lung Cancer!

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PUD Vitals

–Normal majority of the time

–Tachycardia*
•May be due to pain or warning sign for shock due to blood loss •Tachycardia + hypotension even more concerning!

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Lab findings for PUD

Supportive:
•CBC–Anemia
•BMP:–Elevated BUN (BUN-Cr ratio > 36:1)

H. Pylori Testing:
•Fecal antigen test
•Urea Breath test
•Endoscopic biopsy

•DO NOT ORDER SERUM H PYLORI TESTING TO DIAGNOSE ACUTE INFECTION

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Radiology PUD

Plain Film: Rule out perforation by looking for free air under the diaphragm

Barium Study: Falling out of favor, but can detect larger ulcers

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PUD Diagnosis

Endoscopy: Provides both diagnostic and therapeutic solutions to PUD

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Physical Exam Gastroparesis - what to look for

Vitals?
Abd?
Lungs?
Skin?

Vitals:–Normal majority of the time
Tachycardia possible due to pain
Autonomic dysfunction in setting of DMII
Abdomen: –+/-Epigastric pain, +/-distension
Lungs: –Crackles (ILD secondary to scleroderma)
Skin: –Raynaud’s (Scleroderma associated)

Labs and Imaging Gastroparesis

Supportive Labs:
•A1C: Screen with diabetes
•ANA*: Underlying auto-immune condition

Radiology:
•CT abdomen: Ordered initially to rule out mechanical obstruction
•Gastric Scintigraphy:–Nuclear study–Consume radioactive eggs –Take images at 0, 30, 60 and 120 minutes

Gastroparesis treatment

Treat underlying disease
Stop drugs that delay gastric emptying
Dietary modification: Low fat diets, limit non-digestablefiber
Prokinetictherapy

1st line treatment for gastroparesis?

(Prokinetictherapy)
Metoclopramide: Dopamine 2 receptor antagonist, stimulates ACh action in the GI tract, enhancing motility & increasing LES tone

Pancreatitis Physical Exam
vitals?
general?
lung?
abd?

Vitals–Low grade fever, possible
–Tachycardia, very common
–Hypotension, possible

General–Anxious, some level of distress

Lung–Pleural effusions possible

Abdomen: –Epigastric/periumbilical pain, guarding, muscle rigidity
–Hypoactive bowel sounds

Why do we see vitals of
fever, Tachycardia, Hypotension in pt with pancreatitis?

Hypovolemia
Cytokine release
Digestive enzymes in circulation

Grey Turner’s Sign?

bruising on the flanks - pancreatitis

Cullen’s sign?

bruising around the umbilicus - Necrotizing pancreatitis with retro or intraperitoneal bleeding

Panniculitis?

Inflammation of pancreas subcutaneous fat, resulting in necrosis

Diagnostic lab findings - pancreatitis

Diagnostic: •Serum amylase (\> 3x ULN): 67-83% sensitivity •**Serum lipase** ( \>3 x ULN): 82-100% sensitivity

Radiology for pancreatitis

**Abdominal CT: GOLD standard for diagnosis** –Pancreatitis •Necrosis •Abscess •Hemorrhage •Calcifications (chronic) –Pancreatic mass **Plain Radiograph** •Insensitive, not good for detecting pancreatitis •BUT...may show stigmata of disease –Ileus –Pleural effusion **Abdominal Ultrasound** •May reveal signs of pancreatitis –Increased volume of pancreas –Decreased echogenicity •Good for identifying gallstones, thrombosis and necrosis ``` Magnetic resonance cholangiopancreatography (MRCP) Endoscopic Ultrasound (EUS) ```

How do we reach a dx of pancreatitis?

Requires 2 of the 3 following findings: 1. Abdominal pain consistent with pancreatitis 2. Serum lipase or amylase 3 times the ULN 3. CT or MRI imaging findings consistent with pancreatitis

Predictors of negative outcomes - pancreatitis

•Age \> 60 years old •Obesity (BMI \>30) •Long term heavy EtOH use •Labs: –Elevated BUN/Cr = AKI –Hemoconcentration –Elevated inflammatory markers (CRP) •Elevated scoring system (APACHE II)

Is rib raising sympathetic inhibition or parasympathetic inhibition? Why?

Sympathetic inhibition: Initially causes stimulation of the sympathetic activity, but in the long run, rib raising “overrides” the system resulting in prolonged reduction in sympathetic outflow from the area treated

Esophagus chapman's points (ant & post)

Ant: Between rib 2 & 3 parasternally Post: Lateral to T2 spinous process

Stomach Chapmans point (ant & post)

LEFT A: Between Rib 5-6 and 6-7 at costochondral junction P: Lateral to T5 & T6 spinous process

Liver Chapman point (ant & post)

RIGHT A: Between Rib 5-6 and 6-7 at costochondral junction P: Lateral to T5 & T6 spinous process

Gallbladder chapman point (ant & post)

RIGHT A: Between Rib 6-7 at costochondral junction P: Lateral to T6

Pancreas chapman point (ant & post)

RIGHT A: Between Ribs 7-8 at the costochondral junction P: Lateral to spinous process of T7

Small intestines chapman point (ant & post)

A: Between Ribs 8 -11 bilateral at the costochondral junction P: Lateral to spinous processes of T8, 9, 10

Question 1 of 3: 45 y/o male presents to the clinic with chest pain. Symptoms have been present for the past several weeks, but in the last 48 hours pain symptoms have worsened, and he endorses some difficulty with swallowing. Chest pain symptoms seem to be worse while eating and going to bed. Symptoms are not related to strenuous activity. He denies dyspnea on exertion. He does report having a chronic cough. Drinking cold water, temporarily relieves symptoms. Pain is described as dull, intermittent burning sub-sternally. The pain is non-radiating and currently a 4/10 in nature. He attempted to take OTC ibuprofen (800mg) with no relief of symptoms. Which of the following is the most likely diagnosis? A.Peptic Ulcer Disease B.Acute Coronary Syndrome C.Pancreatitis D.GERD E.Gastroparesis

D.GERD

Question 2 of 3: Vital signs are normal. Physical exam is significant for mild epigastric pain but is otherwise benign. CBC and BMP are normal. What is the next best step regarding investigation of the patient’s symptoms? A.No further work-up, start lifestyle modification B.No further work-up, start on PPI C.Endoscopy D.Ambulatory 24-48hr pH monitoring E.CT abdomen

A.No further work-up, start lifestyle modification B.No further work-up, start on PPI Investigation: NoneReserved for patients with no significant GERD alarm features: •New onset symptoms \> 60 years old •New iron deficiency anemia •Dysphagia •Odynophagia •Weight loss •Evidence of bleeding (hematemesis, melena)

Question 3 of 3: Endoscopy reveals LA grade B esophagitis secondary to GERD. An esophageal stricture is also noted and thought to be the cause of the patient’s dysphagia symptoms. What is the best treatment option for this patient? A.Esophageal dilation B.PPI therapy C.H2 blocker D.Lifestyle modification E.Answer A,B,D

E.Answer A,B,D Treatment: GERD, Erosive Esophagitis, esophageal stricture•Strictures need to be dilated to eliminate dysphagia symptoms (Answer A)•GERD can be treated with H2 blockers or PPI therapy, but anytime there’s mucosal damage (esophagitis, PUD) PPI is the preferred treatment. (Answer B)•Patient must address lifestyle modifications in order to attempt trial off medications. These include weight loss, dietary modifications, sleep hygiene. Answer D