GI Block One Flashcards
What does food equal
Chemical energy
What type of system is the GI system
Tubular, with close association to cardio
- Alimentary Nourishment Canal *
Length of GI when alive vs when cadaver
16-23 feet
23-29 feet
due to loss of muscular tone
Muscular alimentary canal main organs (5)
Esophagus Stomach Small Instestine Large Instestine Anus
Accessory digestive organs
Gallbladder
Liver
Pancreas
Six processes of digestion
Ingestion
Secretion
Mixing Propulsion
Digestion
Absorption
Defection
Largest serous membrane in the body and contents
Peritoneum
Simple squamous epithelium with parietal and visceral peritoneum
Organs retroperitoneal
Kidneys Ascending colon Descending colon Duodenum Pancreas
Where does the esophagus begin and end
Laryngopharynx to esophageal hiatus before the stomach
Muscular contents of the esophagus
Superior 1/3 = skeletal ; think UPPER ESOPHAGEAL SPHNICTER
Middle 1/3 = skeletal; and smooth
Inferior 1/3 = smooth ; think LOWER ESOPHAGEAL SPHINCTER
What is the esophageal ole in digestive enzyme production and reabsorption
It has NONE
serves as a mixing chamber and holding reservoir
Stomach
What do parietal cells secrete
Hydrochloric acid and Intrinsic Factor
What do chief cells secrete
Pepsinogen and gastric lipase
How often are peristaltic waves
15-20 seconds
- approximately 3mL of chyme is ejected into the duodenum each wave*
What are the parietal cells role in digestion?
Proton pumps (powered by H+/K+ ATPases) actively transport a H+ into lumen while bringing a K+ into the cell
What does the enzyme carbonic anhydride catalyze?
Formation of carbonic acid from water and co2
Providing a H+ source for proton pumps and bicarbonate
How can HCL be signaled to release from parietal cells (3)
Acetylcholine (ACh) released by parasympathetic neurons
Gastrin being secreted by G Cells
Histamine- paracrine substance released by local mast cells in lamina propria
Pancreatic duct (Duct of Wirsung) does what?
Joins common bile duct from liver and gallbladder then enters duodenum as the hepatopancreatic ampulla (also known as the ampulla of Vater)
Ampulla of Vater is regulated by the sphincter of Oddi
What do acini clusters secrete
Pancreatic juice
How much pancreatic juice is secreted daily
1200-1500mL
Contents of pancreatic juice
Sodium bicarbonate, water, salts, enzymes
What do pancreatic amylase secrete/trypsin?
PA = Starch digestion
Trypsin =Protein digestion
What are the active enzymes vs inactive
Active
Trypsin
Chymotrypsin
CArboxypeptidase
Inactive Trypsinogen Chymotryipsinogen Procarboxypepetidase Proelastase
Where does the falciform ligament extend
extends from undersurface of the diaphragm between the two lobes to the superior surface of the liver
Where does the ligamentum teres extend
extends from falciform ligament to umbilicus
remnant of umbilical vein of fetus
What tow sources feed the liver blood
Hepatic Artery (25%) - 02
Portal Vein (75%) - deoxygenated blood and nutrients
How does blood transfer in the liver
Sinusoids —> Central Vein —> Hepatic Vein —> IVC —> Right atrium of the heart
Hepatocytes grouped together form complex three-dimensional arrangements (wall/slice)
Hepatic Laminae
Liver major functional unit
Hepatic lobules
Four types of metabolism of the liver
Carbohydrate - blood glucose mx
Lipid - fat stores
Protein - ATP production
Drugs and Hormones
Phagocytes of the liver
Kupffer cells
pH of Bile
7.6 - 8.6
Stores and concentrates bile made by the liver (up to 10x’s more concentrated)
Water and ions are reabsorbed by the gallbladder walls
Between meals, bile is made and released by liver into common hepatic duct and down into common bile duct
Gallbladder
Three regions of the small Instestines
Duodenum - shortest region ; retroperitoneal
Jejunum - 3 ft long
Ileum - longest region 6 feet long ; goes to ileocecal sphincter
Methods of absorb toon of the small Intestine
Diffusion
Facilitated diffusion
Osmosis
Active Transport
- 90% of all absorption occurs in the small intestines
(remainder in stomach and large intestines)*
Four regions of large intestine
Cecum
Colon
Rectum
Anal Canal
~5 ft. long, ~2.5inches in diameter
Attached to the posterior abdominal wall by its mesocolon
Opening from the terminal ileum to the large intestine
Allows materials to be passed from small intestine into the large intestine
Ileocecal sphincter
What is the significance of the pectinate line
Above it = innervated by inferior hypogastic plexus; sensitive to stretch ONLY
Below it = innervated by rectal nerves; sensitive to pain temperature and touch
important for hemorrhoids
What is dypepsia and when is it clinically relevant
Acute, chronic, or recurrent pain predominantly located in the upper abdomen (epigastric)
Clinically relevant ≥ 1 month
heartburn
Difference between organic and functional dyspepsia
Organic is associated with a disease and functional is defined as a metabolic process disorder
4 organic causes of dyspepsia
Luminal GI Tract Dysfunction
Medications
Pancreaticobiliary Disorders
Systemic Conditions
Most prevalent cause of dyspepsia
GERD (~20%)
PUD (5–15%)
Investigation of choice for dyspepsia
Upper endoscopy
Causes of indigestion commonly (4)
Overeating, eating too quickly,
High-fat foods,
Stress
Alcohol/Caffeine
What drugs can typically be a cause for organic dyspepsia
Aspirin and NSAIDS
Explain pancreaticobilalry disorders and what should this be distinguished from?
Abrupt onset of epigastric or right upper quadrant pain
Acute/Chronic pancreatitis or neoplasms
Causes due to cholelithiasis or choledocholithiasis should be readily distinguished from dyspepsia
Common systematic conditions for organic dyspepsia
Diabetes mellitus and MI
Most common cause of chronic dyspepsia is functional or organic
Functional
enteric infection
Functional dyspepsia can be one of which things and what other criteria?
Bothersome postpraindal fullness
Early satiation
Epigastric pain/ burning
AND
No evidence of structural dz
Alarm features of dyspepsia (8)
Unintentional weight loss New-onset dyspepsia after age 55 years Dysphagia Persistent vomiting Any overt gastrointestinal bleeding, hematemesis, or melena Family history of esophageal or gastric cancer Iron deficiency anemia Palpable abdominal mass or lymph node
Lab testing for dyspepsia includes findings of what?
H pylori testing (urea breath test, fecal antigen test)
CBC
Electrolytes, liver enzymes, calcium (CMP)
Thyroid Panel
When is abdominal imaging performed
When pancreatic, biliary tract, vascular disease, or volvulus is suspected.
When do we perform gastric emptying studies?
Patients with recurrent nausea and vomiting who have not responded to empiric therapies.
Most important risk factor for gastric cancer
H. pylori
Where does H Pylori reside
adjacent to epithelial cells at the mucosal surface and in gastric pits
Invasive H Pylori testing
Gastric mucosal biopsies
Noninvasive H pylori testing
Fecal antigen [PRIMARY]
Urea breathe test
Serology
First line quadruple therapy
PPI, clarithromycin, amoxicillin, and metronidazole for 10 to 14 days.
In areas of high clarithromycin resistance and/or in patients with penicillin allergy.
Bismuth quadruple therapy
PPI, bismuth subsalicylate (Pepto-Bismol), tetracycline, and metronidazole for 10 to 14 days.
What does Metoclopramide do
decreases gastric emptying time
What is rumination
the chewing and swallowing of volitionally regurgitated food
4 causes for vomiting
Afferent canal fibers from the GI viscera
Stimulation of fibers of the vestibular system
Higher central nervous system centers (amygdala)
The chemoreceptor trigger zone
What type of receptors are in the fibers of the GI viscera
Serotonin
Acute onset of nausea without abdominal pain could be?
Food poisoning
Acute gastroenteritis
Systemic illness
Acute onset of nausea with abdominal pain could be?
Peritoneal irritation
Acute gastric obstruction
Pancreaticobilliary dz
Constipation is associated with what?
Hardened feces or underlying disorder
2 top common causes of constipation
Inadequate fiber
Poor hydration
What type of meds cause constipation most
Opioids
Constipation PE finding
Dullness to percussion in left quad
DRE
Who qualifies for A FULL work up for constipation symptoms.
50 years old
Severe constipation
Signs of an organic disorder
Alarm symptoms
What are constipation alarm symptoms
hematochezia, weight loss, positive FOBT
family history of colon cancer or inflammatory bowel disease
What are the lab studies for consitpation
Complete blood count
Serum electrolytes (CMP)
Thyroid panel
Fecal occult blood test
What do radiographs show in a constipation work up
Abdominal non specific bowel gas pattern
Two types of endoscopy for constipation
Colonoscopy or flexible sigmoidoscopy
ConstipationTxM
Dietary fiber
Water
Probiotics
Toilet habits
Regular exercise
What are the osmotic laxatives
Magnesium hydroxide (Milk of Magnesia, Epsom Salts)
Polyethelyne glycol 3350 (Miralax)
**Polyethelyne glycol (GoLYTELY)
**Magnesium citrate
What are the stimulant laxatives
Bisacodyl (Dulcolax)
Senna (ExLax)
What are the stool surfactants
Docusate sodium (Colace)
What is fecal impaction
paradoxical “diarrhea”
Passage of liquid stool around the impacted feces
**can use enemas or DRE to BREAK IT UP*
Long term straining at the stool may result in chronic dilation of the veins of the rectum.
Also known as….?
Hemorrhoids
Acute diarrhea in adults is characterized by 1 of the following occurring in 1 day:
loose or watery stools 3 or more times,
the passage of greater than 200 g of stool,
Most often caused by viruses, but may be caused by bacteria and parasites (to a lesser degree)
Results in milder disease
Non inflammatory diarrhea
Caused by bacteria (invasive and/or toxin producing)
More severe disease; likely to disrupt mucosal integrity
Bloody diarrhea alone or dysentery (ie, bloody diarrhea with fever, abdominal pain, and rectal tenesmus) may be present
Inflammatory Diarrhea
Acute vs chronic
Inflammatory vs non inflammatory
Acute – Less than two weeks
Chronic – Longer than four weeks
Bloody vs Non bloody
Diarrhea between 2 and 4 weeks
Persistent
Things to ask about acute diarrhea
Bloody vs. watery (non-bloody) Recent travel Diet changes (new restaurant) Recent antibiotic use Sick contacts
What are signs of dehydration
Dizziness, light-headedness, orthostatic hypotension
Most common viral causes of inflamm diarrhea
Norovirus (50%)
Rotavirus (children, older adults)
Cytomegalovirus (AIDS)
Less common bacterial causes of inflamm diarrhea
Clostridum perfringens, Bacillus cereus, Staphylococcus aureus
Shiga toxin–producingEscherichia coli
Vibrio choleraetoxin (causes the small intestinal cells to secrete, rather than absorb, fluid and electrolytes)
Parasites than can cause inflamm diarrhea
Giardia, Cryptosporidium, Cyclospora, Cystoisospora belli
How do drugs cause inflamm diarrhea
Drugs can disrupt the mechanisms of mucosal permeability, transport, motility, and gut metabolism
Essentials of diagnosis for acute inflamm diarrhea
Drugs can disrupt the mechanisms of mucosal permeability, transport, motility, and gut metabolism
Diagnostic veal of acute inflamm diarrhea
Routine stool bacterial cultures (including E coli O157:H7)
Testing as clinically indicated for Clostridium difficile toxin, and ova and parasites.
Symptoms of acute inflamm diarrhea
Loose, bloody stools Lower in volume Fever Severe abdominal cramps (LLQ) Urgency Tenesmus
Differential diagnosis for infectious acute inflamm most common
Salmonella
When do you get labs for non inflamm diarrhea
If persist longer than 7 days
What WBC count is concerned for acute diarrhea
15,000/mcL or more
What are the fecal leukocytes likely in non inflamm diarrhea
Negative
How many samples do you need for ova and parasites
3
What is a marker of intestinal inflammation
Fecal Lactoferrin
General diet strategies for diarrhea Txm
BRAT diet (soft, easy to digest foods) Avoid high-fiber foods, fats, dairy, caffeine
Rehydration
Oral Rehydration Salts (ORS)
IV for severe cases
Antimotility agents
Loperamide (Immodium)
Do not prescribe for bacterial or inflammatory diarrhea with blood in stool, or for febrile patients
Bismuth subsalicylate (Pepto-Bismol) Good for traveler’s diarrhea by virtue of its anti-inflammatory and antibacterial properties.
When should you GIVE ABX for acute diarrhea Txm
Shigella infxn
Recent travel pts with 38.5 degrees or higher
Immunocomp’s
Severe hospitalized diarrhea (C diff)
Drug of choice for diarrhea
Fluoroquinolones – drugs of choice
Ciprofloxacin 500 mg BID for 5-7 days
Ofloxacin 400 mg BID for 5-7 days
Levofloxacin 500 mg QD for 5-7 days
Other meds for acute diarrhea Txm
trimethoprim-sulfamethoxazole 160/800 mg BID
doxycycline 100 mg BID
Define travelers diarrhea
Diarrhea that develops during travel or within 10 days of return
Meds for travelers diarrhea
Fluoroquinolones – 3 day courses
Not useful for travel to Southeast Asia
Azithromycin – 1000mg single dose
Rifaximin 200 mg TID x 3 days
ABX is rec for what specific types of diarrhea
Shigellosis Cholera Extraintestinal salmonellosis Listeriosis Traveler’s diarrhea C difficile Giardiasis Amebiasis
What are signs of severe infection or sepsis
temperature higher than 39.5°C, leukocytosis, rash
What are signs of hemolytic uremic syndrome
acute kidney injury, thrombocytopenia, hemolytic anemia
Osmotic diarrhea
Stool volume decreases with fasting
Increased stool osmotic gap
- consider carb malabsorption*
- Consider factitious diarrhea(laxative antacid)*
What is a secretory condition in chronic diarrhea
Increased intestinal secretion or decreased absorption
High volume, watery stool
Little to no change with fasting
Normal stool osmotic gap
**consider factious diarrhea, endocrine tumors, bile salt malabsorption*
Chronic diarrhea inflammatory conditions
Fever, hematochezia, abdominal pain
Consider IBS ; crohns and ulcerative colitis
Examples of motility disorders in chronic diarrhea
Postsurgical
Systemic disorders (eg, DM, hyperthyroidism)
Irritable bowel syndrome
Young adults
Chronic infections that can cause chronic diarrhea
Parasitic infx
Giardia, E histolytica, and Cyclospora
Intestinal nematodes
Systemic conditions that can cause chronic diarrhea
Thyroid disease
Diabetes
Chronic diarrhea most common causes
Meds, IBS, lactose intolerance
Lab tests and stool studies for chronic diarrhea
Lab Tests:
CBC, Chem 17, LFT, Thyroid studies, ESR, CRP
Stool studies:
Culture, Leukocytes, Lactoferrin, Occult blood, O&P, electrolytes
What type of colonoscopy is recommended for chronic diarrhea in severe cases
Colonoscopy with biopsy
To exclude IBD and neoplasm
Overt bleeding from where = GI hemorrhage
Upper GI tract (esophagus, stomach, and duodenum)
Lower GI tract (colon)
Obscure locations (small intestine)
Occult bleeding
widens the angle of the duodenojejunal flexure, allowing movement of intestinal contents
The ligament of Trietz
Suspension muscle of duodenum
Ways to describe upper GI bleed
Hematemesis
Varying degrees of hypovolemia
+/- Melena (may be hematochezia in massive bleed)
Bleeding proximal to the Ligament of Treitz
Most common cause of upper GI bleed
Peptic Ulcer Disease (PUD) – 40%
Portal Hypertension – 10-20%
Esophageal Varices – high mortality rate
Mallory-Weiss Tear
Longitudinal tears in the mucosa of the esophagus
Typically due to forceful retching or vomiting
Strong association with alcohol abuse
Rupture of the esophagus due to forceful retching
Also associated with alcohol abuse
Boerhaave syndrome
what vascular anomalies are associated with upper GI bleeds
Angioectasias
Telangiectasias
First and most important step for assessment and stabilization of hemodynamic status
Stable or Unstable
What is octreotide, when is it indicated?
Consider octreotide if patient has liver disease or portal hypertension
Reduces splanchnic blood flow and portal BP
Unstable Upper GI bleed
What are high risks for upper GI bleeds
Age > 60 Comorbid illnesses SBP < 100 mmHg Pulse > 100 bpm Bright red blood in NG aspirate or upon rectal examination
Pharmaco recommendations for acute management of upper GI bleed
PPI = DOC
Octreotide
Stop NSAIDs
ABX for H. Pylori
Arterial bleed non bleeding visible vessel or clot ; combo endoscopic hemostasis gets what Txm?
IV bonus and infusion PPI for 72 hours
Oozing without other stigma; hemoclip or thermal coat hemostasis gets what Txm?
Oral PPI twice daily
Flat spot or clean base ulcer gets what Txm?
Oral PPI and early discharge
Bleeding distal to the Ligament of Treitz
Majority of lower GI bleeding from the colon
Typically lower risk of serious blood loss than in upper GI bleeding
Lower GI bleed
Most common mild and severe etiology for acute lower GI bleed
Mild = Anorectal Dz ; hemorrhoids, fissures, ulcers
Severe = painless bright red blood ‘’large’’ volume
What etiology is common in patients over 70 years old for acute lower GI bleed
Angioectasis
Most likely causes of lower GI bleed form pts less than 50
Anorectal Disease
Inflammatory Bowel Disease
Infectious Colitis
Most likely causes of lower GI bleed form pts older than 50
Diverticulosis
Malignancy
Angioectasias
Ischemic Colitis
Abdominal pain and cramps is usually due to
IBD
Colitis
Large volume blood loss is commonly what type of bleed
Diverticular
What is an ominous lab finding where Val lower GI bleed
Anemia
First thing to exclude in diagnostic bleeding testing
UPPER GI SOURCE
Large volume w/in 24 hours if active bleed, 24-36 hrs if stable no active bleed; what test is warranted?
Colonoscopy
Small volume diagnostic test
Anoscopy and sigmoidoscopy
Hemodynamically unstable and hmatochezia diagnostic test
Technetium scan and angiography
Txm for large volume bleed
Therapeutic colonoscopy
Intra-arterial embolization
Surgery
persistent or recurrent bleeding, despite negative initial GI evaluation, unknown origin but commonly from small intestine
Obscure GI bleed
Overt GI bleed
melena, maroon stool, or hematochezia
Occult GI bleed
positive result of fecal occult blood testing, usually in the setting of iron deficiency anemia
How do you ID occult GI bleeding
Fecal Occult Blood Test
Fecal Immunochemical Test
More accurate, but only detects lower GI bleed
Presence of unexplained anemia on CBC
ID FOR NEOPLASM
Asymptomatic w/ incidental +FOBT/FIT but no anemia =
colonoscopy
Symptomatic w/ either +FOBT/FIT or unexplained anemia =
upper endoscopy and colonoscopy
When do you get a capsule endoscopy
Occult bleeding or iron def
Bright red blood is what source
Left colonic source
Brown stools mixed or streaked with bright red
Rectosigmoid or anus
Maroon stool source
Small Instestine or right colonic source
Black (Melina) blood source
Upper GI
Largest serous membrane in the body
Peritoneum
What type of tissue is the peritoneum
Consists of a layer of simple squamous epithelium (mesothelium) with underlying layer of areolar connective tissue
Common causes of ascites
Liver dz = 80%
Hepatic congestion
Hypualbuminemia
Functions of the hepatic portal system
supplies the liver with metabolites
ensures that ingested substances are processed in the liver before reaching the systemic circulation
What is defined as pathological increase in portal pressure
Pressure gradient increase in portal pressure between portal vein and IVC > 10 mmHg
How can liver dz lead to ascites?
Cirrhosis —> increased intrahepatic vascular resistance ————->increased capillary pressure —->increased hepatic lymph formation —->ascites
What can lead to ascites
Alcohol abuse
Risk factors for Hepatitis
History of malignancy (cancer)
Signs of portal HTN and liver dz
Hepatic enlargement (+/- tenderness) Elevated JVP Large abdominal wall veins
Liver dz
Muscle wasting
Malnourishment
W/ FEVER = BACTERIAL PERITONITIS
Shifting dullness test
a change in the location of dullness to percussion when the patient is turned due to movement of the ascites
Lab tests and what studies are collected
Abdominal paracentesis
Inspection
Cloudy infection; Milky chyle; Bloody traumatic/malignant
Studies
White cell count
Albumin and total protein* (SAAG)
Culture and Gram stain
Formula for serum-ascites albumin gradient
(serum albumin) – (ascitic fluid albumin) = SAAG
≥1.1 g/dL = portal hypertension
<1.1 g/dL = non-portal hypertension cause
Good imaging studies for ascites
US and CT
What must you distinguish ascites from?
Inter abdominal infx from secondary bacterial peritonitis
Spontaneous bacterial peritonitis common path’s (5)
E coli Klebsiella pneumonia Streptococcus pneumonia viridans streptococci Enterococcus species
What is the TTP associated with spontaneous bacterial peritonitis
Abdominal pain WITHOUT focal tenderness to palpation
MOST. Important lab test eval of ascetic fluid via paracentesis (2)
And if you suspect secondary bacterial peritonitis
Gram stain and culture
Cell count with differential
Abdominal CT
Empiric TXM for spontaneous bacterial peritonitis
IV 3rd generation cephalosporin (eg, cefotaxime or ceftriaxone)
Combination beta-lactam/beta-lactamase agent (eg, ampicillin/sulbactam
What is good prophylaxis for pts who survive an episode of sponataneous bacterial peritonitis
Once daily oral ABX
Define malignant ascites
Due to carcinoma of a peritoneal organ
Blocked lymphatic channels as a result of malignancy
direct production of fluid into the peritoneal cavity by highly active cancers
Chylous ascites
Accumulation of lipid-rich lymph (chyle) in the peritoneal cavity
Milky white in appearance
Due to lymphatic obstruction (lymphoma)
Pancreatic ascites
intraperitoneal accumulation of massive amounts of pancreatic secretions
Due to disruption of pancreatic duct
Seen in chronic pancreatitis
Bile ascites
Due to complications from biliary tract surgery, or percutaneous liver biopsy, or abdominal trauma
TB peritonitis
Rare in the US – may encounter during deployment
Active TB infection with peritoneal involvement
General signs and symptoms of esophageal dz
Heartburn (pyrosis)
Dysphasia (can’t swallow)
Odynophagia (painful swallow)
Study of choice for esophageal dz
Upper Endoscopy (EGD)
When do we perform barium esophagograpahy
To differentiate b/w structural and motility issues
What tests function of lower esophageal sphincter
Manometry
GERD is a disfx of what?
LOWER esophageal sphincter
What it’s the squamous columnar junction
Lower Esophagus and stomach meeting point
What it’s the correlation of severity and tissue damage
THERE ISNT ONE
ALARM FEATURES of GERD
Troublesome dysphagia Odynophagia Weight loss Iron deficiency anemia Fever, chills, night sweats
What can be visualized with the EGD
Esophagus, stomach, duodenum
What type of foods precipitate reflux
Fatty foods, chocolate, peppermint, alcohol
Mild GERD Txm
PRN OTC antacids or H2
Troublesome symptoms TXM of GERD
PPI daily
If symptoms persists more than 4 weeks on daily PPI
Switch to BID dose
Characteristics of OTC Antacids
Rapid relief, short duration of action
H2 Receptor antagonists and pharmacotherapy
-tidine
Cimetidine (Tagamet), Ranitidine (Zantac), Famotidine (Pepcid)
Onset of action is 30 minutes, duration is 8 hours
Can be taken before meals to prevent onset of symptoms
PPI’s dosing and efficacy to H2
-prazole Omeprazole (Prilosec) 20 mg Rabeprazole (Aciphex) 20 mg Lansoprazole (Prevacid) 30 mg Esomeprazole (Nexium) 40 mg Pantoprazole (Protonix) 40 mg
Once daily dosing; 30 mins before breakfast
Superior to H2’s
When can you discontinue PPI’s
8-12 weeks
most will need continued therapy
Nissan Fundoplication Surgical Summary
fundus of the stomach is wrapped around the esophagus and sewn into place so that the lower portion of the esophagus passes through a small tunnel of stomach muscle
REINFORCES THE LES
Squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium containing goblet and columnar cells
Result of prolonged exposure to caustic gastric contents
BARRETT Esophagus
What can Barrett esophagus do to symptoms of GERD
Reduce
Association between GERD and esophageal adenocarcinoma
11-fold increased risk of esophageal adenocarcinoma
PPI therapy
surveillance endoscopy w/ biopsies every 3–5 years
Narrowing of the esophageal lumen at the GEJ
Progressive solid food dysphagia
Treated with endoscopic dilation
Peptic stricture
What are the diff types of esophagitis
Infectious
Pill-induced
Eosinophilic
What empiric antigunfal can be used for infxn esophagitis
Fluconazole (Diflucan) if no response in 5 days EGD
Inflammatory response of the esophagus to allergen (food or environmental)
Eosinophilic esophagitis
Leads to progressive dysphagia
What history should you ask about for EO EOsophagitis
Asthma
Allergies
Atopic Dermatitis
Clinical findings of EO Esophagitis
Dysphagia to solid foods
Heartburn
Txm of EO Eosinophilic esophagitis
Empiric trial of PPI first BID dosing for 2 months Referral to allergist Topical corticosteroids Swallowed fluticasone (from inhaler)
Esophageal webs
Thin mucous membrane of squamous epithelium
Mid to upper esophagus
Most are asymptomatic
May cause intermittent dysphagia or GERD like symptoms
Esophageal rings (Schwarzkopf Rings)
Circumferential mucosal structure in the distal esophagus
Similar symptoms as webs
Strong association with hiatal hernia
Diagnostic test and Txm of esophageal webs and rings
Diagnostic test
Barium swallow
Treatment
Endoscopic dilation if symptomatic
Zenker diverticulum and symptoms?
Pharyngoesophageal diverticulum
‘pharyngeal pouch’
Symptoms Progressive dysphagia Sensation of food ‘sticking’ in the throat Halitosis Regurgitation of undigested food, pills
How do you diagnose zenker
Barium swallow
Achalasia and etiology
Esophageal motility disorder
Loss of normal peristalsis in the distal 2/3 of the esophagus
Impaired relaxation of the LES
ETIOLOGY Idiopathic (autoimmune, viral, or primary neurodegenerative processes suspected)
Main symptom of Achalasia
Progressive dysphagia to solids and liquids
What deformity is associated with Achalasia
Birds beak
Chagas
parasitic disease caused by Trypanosoma cruzi
Endemic to Mexico and South & Central America
Inquire about travel history
similar to Achalasia
Txm of Achalasia
Botulinum Toxin into the LES – 85% effective, 50% relapse, preferred for poor surgical candidates
Pneumatic dilation – preferred, 90% effective
Surgery - 95% effective
Dilated submucosal veins due to portal hypertension
Over 50% with cirrhosis
Cause severe upper GI bleeding
High mortality rate
Esophageal varices
Follow on Txm of esophageal varices
Reduction of portal hypertension
Beta blockade (propranolol)
Variceal band ligation
Mucosal tear at the GEJ
Mallory-Weiss Syndrome
Sudden increase in abdominal pressure
Retching or vomiting
Strong association with alcoholism
Pt presents with hematemesis
TxM of Mallor-Eiss Syndrome
Endoscopic hemostatic agents Vasoconstrictive agents (epinephrine) Cautery Endoclip
Complete rupture of the esophagus
BOERHAAVE SYND
Rare form of cancer
3:1 male to female ratio
May be squamous cell or adenocarcinoma
Esophageal carcinoma
S and S of esophageal carcinoma
Progressive solid food dysphagia
Odynophagia
Significant, unexplained weight loss
May be body aches or pains associated with metastasis
What establishes diagnosis of esophageal carcinoma
EGD
Type I: Sliding hernia:
Displacement of the gastroesophageal junction above the diaphragm.
The stomach remains in its usual longitudinal alignment and the fundus remains below the GE junction
Type II, III, IV: Paraesophageal hernias:
True hernia with a hernia sac
Upward dislocation of the gastric fundus through a defect in the phrenoesophageal membrane
Diagnosis and TXM of Hiatal Hernia
Diagnosis
Barium swallow
Treatment
Small hernias GERD management
Larger hernias surgical repair
Gastropathy vs Gastritis
Gastropathy – mucosal damage without inflammation
Gastritis – mucosal damage with inflammation
What irritants are assoc with gastropathy
Alcohol
NSAIDS
Need mucosal biopsy for diagnosis
Less common etiologies of Erosive Hemorrhagic gastropathy
Physical stress
Portal HTN
S and S of Erosive and Hemorrhagic Gastropathy
General Symptoms and Signs
Patient may be asymptomatic
When symptomatic:
Anorexia
Epigastric pain
Most common clinical manifestations of Erosive and Hemorrhagic Gastropathy
Upper GI bleed
What do prostaglandins do?
Play a key role in the generation of the inflammatory response
Inflammation is the immune system’s response to infection and injury
Describe gastric prostaglandins
Stimulate epithelial cells to release more bicarbonate and mucus
Act as potent vasodilators
NSAID gastropathy most common s and s and Treatment
Dyspepsia
TXM = stop NSAID
If you have to continue NSAID Txm what should you due to decrease risk of NSAID gastropathy
Ensure medication taken with milk or meals
Add daily PPI
How does alcoholic gastropathy occur
Ethanol has direct toxic effect on gastric mucosa
It also impairs gastric motility and leads to delayed gastric emptying
Txm of alcoholic gastropathy
Treatment with discontinuation of alcohol and
H2 or PPI for 2-4 weeks.
What prophylaxis can be given for stress gastropathy
Prophylactic H2-receptor antagonists (intravenous) or proton pump inhibitors (oral or intravenous
Stress gastropathy is associated with bleed if what else is present
Coagulopathy
Respiratory failure w/ mechanical ventilation
Txm of portal HTN gastropathy
beta blockade to
lower portal pressure.
What type of inflitrtation happens with H pylori gastritis
Neutrophilic and lymphocytic infiltration
When do we test for H. Pylori
dyspeptic patients
chronic GERD patients
suspected or confirmed PUD patients.
What do use to test post treatment eradication
Fecal antigen
What should be discontinued before H. Pylori testing
anti-secretory therapy for 2 weeks prior to testing
When do we perform H pylor test of cure
4 weeks post TXM
Standard Bismuth Quad therapy
PPI PO twice daily
Bismuth subsalicylate 262mg - two tablets PO four times daily
Tetracycline 500mg PO four times daily
Metronidazole 500mg PO three times daily
Standard Non bismuth Quad Therapy
PPI PO twice daily
Amoxicillin 1000mg PO twice daily
Metronidazole 500mg PO twice daily
Clarithromycin 500mg PO twice daily
Standard Triple Therapy (in lower than 15 % resistance)
PPI PO twice daily
Clarithromycin 500 mg PO twice daily
Amoxicillin 1 g orally PO twice daily
(or metronidazole 500 mg PO BID, if PCN allergic)
Menetrier Dz
Idiopathic hypertrophic gastropathy
Nausea, epigastric pain, weight loss, diarrhea
Peptic Ulcer
A break in the gastric or duodenal mucosa
Due to impaired mucosal defense mechanisms
Types of ulcers associated with age
Duodenal ulcers
More common in younger patients (30-55)
Gastric Ulcer
More common in older patients (55-70)
Difference between s and s of gastric vs duodenal ulcers
Shortly after eating with gastric ulcers
2-4 hours after eating for duodenal ulcers
Pain with eating gastric duodenal
Gastric - Increase
Duodenal - Decrease
Work up for PUD
EGD establishes the diagnosis
Refer suspected PUD patients for endoscopy
Labs CBC – check for anemia FOBT – eval for occult bleeding H pylori If PUD is found on endoscopy, biopsy will be taken
Txm goals of PUD (4)
Relieve dyspepsia
Promote ulcer healing
Eradicate H pylori infection, if present
Prevent recurrence
PUD Txm NSAID
Discontinue if possible
Titrate to lowest effective dose
Switch to COX-2
Treatment of PUD first line
PPI’s
Mucosal defense adjunct treatment meds (2)
Sucralfate (Carafate) – forms viscous protective coating at sites of ulceration
Misoprostol (Cytotec) – prostaglandin analog
Often given as prophylaxis for long term NSAID patients
Downside – administered 4x/day and causes diarrhea in 10-20%
Common complication of PUD
Acute upper GI hemorrhage
Ulcer perforation
S and s of ulcer perforation
Sudden, severe abdominal pain
Rigid abdomen, reduced bowel sounds, + rebound ttp
Pneumoperitoneum
(Air under the diaphragm)
Surgical repair of ulcer perforation if
Evidence of free abdominal air or peritonitis
Deterioration of patient while admitted
Ulcer penetration
Penetration of the ulcer through the bowel wall without free perforation or leakage of luminal contents into the peritoneal cavity
Common places that ulcers penetrate
Pancreas, liver, biliary tree
What symptom change is key for ulcer penetration diagnosis
Change in dyspepsia = increased
Lack of relief with foods or antacids
Gastric outlet obstruction
Chronic edema of pylorus or doudenal bulb
Symptoms of gastric outlet obstruction
Early satiety
Postprandial vomiting (undigested food contents)
Weight loss
Treatment for gastric outlet obstruction
Correct electrolyte embalance
High dose PPI
Endoscopic dilation
Gastrin-secreting neuroendocrine tumore
Gastrinoma (Zollinger Ellison)
What is the gatrinoma triangle
Junction of common and cystic duct
Pancreatic neck
3rd portion of the duodenum
Commonalities of Zollinger Ellison syndrome gastrinoma
G locations
Pancreas
Duodenal wall
Lymph nodes
common in patients with MEN-1
What do Zollinger Ellison syndrome pts develop 90% of the time
PUD
When do you screen for Gastrin levels
In patients with refractory ulcers or in patients with PUD and family history of MEN1
In patients with PUD who are not taking NSAIDS and are H pylori negative
Gastroparesis.
Delayed gastric emptying in the absence of a mechanical obstruction
Most common associated dz cause of gastroparesis
Diabetes Mellitus
Cardinal symptoms of gstroparesis
Nausea Vomiting Early satiety Bloating and/or upper abdominal pain Weight loss in severe cases
What type of gastroparesis reps NG decompression and IV fluid/ electrolyte replacement
Acute exacerbations
General Txm of gastroparesis
Diet changes
Glycemic control in DM pts
Prkineteic Meds = Metoclopramide (Reglan)
Domperidone
Erythromycin
Classic signs of metastatic gastric adenocarcinoma
Sister Mary Joseph Nodule
Virchow node
Diagnostic studies of Gastric Adenomcarcinoma
Labs
CBC often shows anemia
LFTs may be elevated
Endoscopy
Confirms diagnosis
Other radiographs
CT, PET once cancer is confirmed to find mets.
Secondary tumor from spread of non Hodgkin lymphoma
Gastric lymphoma
What type of tissue arises from MALT
Mucosa associated lymphoid tissue
Chronic H pylori
Carcinoid tumor vs carcinoid syndrome
Carcinoid tumor - neuroendocrine tumors originating in the digestive tract or lungs
Carcinoid Syndrome - constellation of symptoms mediated by various humoral factors that are elaborated by some carcinoid tumors
3 symptoms of carcinoid syndrome
Cutaneous flush
Venous telangiectasis
Diarrhea (watery no blood, abdominal cramps)
Classic child pyloric stenosis
3-6 week old child
Immediate postprandial projectile vomiting
Fussy and hungry immediately after meals
Constipation, dehydration
Where do you palpate the infantile hypertrophic pylori stenosis
Palpation of “olive” in the right upper quadrant
Hypertrophic pylorus
Signs and symptoms of malabsorption disorders
Steatorrhea = bulky greasy stools that FLOAT
Microcytic/Macrocytic anemia = iron b12 folate malabsorption
Diary intolerance = lactase deficiency
What is celiac dz
Gluten sensitive enteropathy
Immune response
=diffuse damage to proximal small intestinal mucosa
S and s of celiac disease (4)
Dyspepsia
Diarrhea
Steatorrhea
Borborygmi (loud stomach sounds)
Extra instinct manifestations (4)
Fatigue
Depression
Transaminitis
Dermatitis herpetoformis
Dermatitis herpetiformis
Prurience Papuans nad vesicles of extensor surfaces; trunk scalp, neck.
Lab testing for celiac
CBC
CMP
UA
Specific celiac serology (IgA and IgG)
What is IGA tissue transglutaminase antibody
IgA tTG
Test of choice in Celiac ID
Serum IgA levels can reveal undiagnosed IgA deficiency
IgG-deamidated gliadin peptides (DGPs)
ID’s patients with IgA deficiency
IgA
Most abundant antibody protects mucosal tissues form microbial invasion and maintains homeostasis
What is the confirmatory test for celiac dz diagnosis
Mucosal biopsy of proximal and distal duodenum
W/ Histological blunting and/or atrophy of the intestinal villi
(Villous Atrophy)
Can you eat oats with celiac disease
NO!
What do celiac patients have a SLIGHT increased risk for?
Lymphoma and adenocarcinoma
Whipped disease
Rare multisystem illness caused by infection with the Bacillus Tropheryma whippelii
Seen mostly in farm or sewage workers
Contact with sewage/waste water
Fatal if untreated
Classic presentation of whipple dz
Migratory arthralgias (Large joint involvement) Diarrhea Abdominal pain Weight loss Fever
What are less common signs of whipple dz (4)
Skin hyperpigmentation
Generalized lymphadenopathy
Ophthalmoplegia
Nystagmus
How do you diagnose whipple dz
Evidence of bacterium in mucosal biopsy sample
“Foamy macrophages”
Treatment of whipple dz
IV ceftriaxone x 2 weeks
TMP-SMX DS – 1 tab po BID x 12 months
Tropical spruce
Environmental enteropathy; tropical malabsorption
Chronic diarrheal disease, possibly of infectious origin
Often seen following acute diarrheal disease
Entire small Instestine involvement
Malabsorption of folic acid and B12
S and s of tropical spue
“Inflammation of the Mouth”
Chronic diarrhea Steatorrhea Weight loss Anorexia Malaise B12 and Folate deficiency Glossitis & chelitis
Findings of endoscopy in tropical sprue
Gross findings
flattening of duodenal folds
Microscopic findings
shortened, blunted villi and elongated crypts with increased inflammatory cells
How do you prevent and treat tropical sprue
Prevention
Boil/bottled water
Peel fruits before eating
Treatment
TMP-SMX x 6 months
Folate, B12 supplementation
Explain lactase deficiency
Lactase = brush borer enzyme that hydrolysis lactose into glucose and galactose
Malbosrbed lactose is fermented by intestinal bacteria = gas and organic acids
S and s of lactase deficiency
“Dose dependent”
Small intake —>may be asymptomatic
Moderate intake —> bloating, abdominal cramps, and flatulence
Large intake —> osmotic diarrhea
Diagnostic test of lactase deficiency
Hydrogen breath test
What patients should you be concerned with bacterial overgrowth
Are on chronic PPI therapy
Due to gastric achlorhydria
Have an anatomic abnormality of the small intestine
Suffer from a small intestine motility disorder
May have a gastrocolic or coloenteric fistula
Bacterial overgrowth main symptoms
Steatorrhea
Macrocytic anemia
Treatment of bacterial overgrowth
Ciprofloxacin
Amoxicillin-clavulanate
Rifaximin
Short bowel syndrome
Removal of significant segments of the small intestine
Acute paralytic ileus
A dynamic = post op
Failure of peristalsis
Hospitalized patients due to
surgery
severe illness
meds of motility = opioids, anticholinergics
Main symptoms of acute paralytic ileus (4)
Diffuse constant abdominal pain
Lack of abdominal TTP
Absent/Low bowel sounds
Abdominal distention
Diagnostic testing
Non specific electrolytes and X-ray ID
Txm of acute paralytic ileus
Treatment of underlying illness
Pain management
Fluid maintenance & electrolyte replacement
Bowel rest
Nasogastric decompression
For patients with significant distension or severe vomiting
Chronic intestinal pseudo obstruction
Similar to Gastroparesis
Signs of obstruction without actual obstruction
Work up for chronic intestinal pseudo obstruction
CT or endoscopy
NG decompression and IV fluid/electrolyte replacement
What is small bowel obstruction most commonly attributed to
postoperative adhesions or hernias
Clinical presentation of small bowel obstruction
Colicky abdominal pain Nausea Profuse vomiting Obstipation Inability to pass flatus or stool
Small bowel obstruction physical exam
Abdominal distension
Tympany on percussion
Hyperactive bowel sounds early
Hypoactive later on
Signs of dehydration
Lab test for small bowel obstruction
CBC CMP Urinalysis Type and crossmatch If surgery may be indicated
Radiographs of small bowel obstruction show what
Plain abdominal films
Both upright and supine
Dilated loops of small bowel with air-fluid levels
What does a CT scan ID in small bowel obstruction
strangulated obstruction
Small bowel obstruction treatment - ACUTE (6)
Fluid resuscitation Bowel decompression (NG) Pain control Anti-emetic medications Early surgical consultation Admission
What is the precession of strangulated bowel obstruction
Dilation —> Compromise of the intramural vessels of the small intestine —>Ischemia —>Necrosis —>Bowel perforation —>Sepsis
Gallstone ileus
Complication of cholelithiasis.
Due to impaction of a ≥2cm gallstone in the ileum after being passed through a biliary-enteric fistula
What dz can cause intussusception
Mencken diverticulum
Triad of intussusception classic symptoms
colicky abdominal pain, vomiting, “currant jelly stools
Txm of intussusception
Pneumatic Reduction of air with flouroscope
Hydrostatic reduction with saline with US or flour
Surgery
Neoplasm of the small bowel may cause
Intussusception and obstruction
Small intestinal neoplasms (4)
Adenocarcinoma
Lymphomas
Intestinal carcinoid
Sarcoma
Protein losing enteropathy
Excessive loss of serum protein in the GI tract
=hypoalbuminemia
Established GI disorder
Mesenteric ischemia
Interruption of blood flow to the bowel
- arterial occlusion
- venous thrombosis
- non-occlusive (vasospasm, low cardiac output)
PE finding common with mesenteric ischemia
Classically = “pain out of proportion with physical exam”
Diagnostic test of mesenteric ischemia
CT angiography
TxM of Mesenteric Ischemia
Papaverine – smooth muscle relaxant
Thrombolytics
Surgical referral
Rule of twos for meckels (6)
Occurs in 2% of the population 2:1 Male-Female ratio Located within 2 feet of ileocecal valve 2 cm in length 2 types of mucosa Native intestinal mucosa and heterotopic mucosa (most commonly gastric or pancreatic) Symptoms commonly occur before age 2
Clinical presentation of meckels
GI Bleeding – due to heterotopic gastric mucosa (acid-producing tissue - may lead to ulcers and bleeding)
Abdominal Pain – most common anatomic location may present similarly to acute appendicitis
Diagnosis of meckels
Capsule Endoscopy
Meckel’s Scan:
nuclear medicine study using 99m technetium pertechnetate, which has an affinity for gastric mucosa
TxM of meckels
Surgery Referral
Asx = no treatment
Sx = stabilize the bleed, surgical removal, correct intussusception if present
True diverticulum of the cecum
Appendix
Attachment at the base of Cecum
Appendix locations
Retrocecal Subcecal Preileal Postielal Pelvic
Pathogenesis of appendicitis
Obstruction —>increased pressure —>venous congestion ——->infection —>necrosis
Fecalith
Hard stony mass of feces
How long until untreated necrotic appendix leads to sepsis?
36 hours
Clinical presentation of appendicitis
Early - Vague, colicky periumbilical pain
Later (within 12 hrs) – pain migrates to RLQ
McBurney’s Point
Pain is sharp and increased with peritoneal irritation
Coughing, jumping, “bumpy ride”
Patient will be lying still
Where can the migration of cecum during pregnancy cause pain in appendicitis
Right flank
Right subcostal
Physical exam findings of appendicitis
TTP at Mcburneys Point
Direct AND Rebound tenderness
Guarding
Rigidity
Signs of peritoneal irritation
Heel tap (pain worsened by walking or coughing)
Psoas sign (pain on passive extension of right hip)
Obturator sign (pain with passive flexion and internal rotation of the right hip)
Rovsing’s Sign (palpation of LLQ elicits pain in the RLQ
What is the CBC finding of appendicitis
Moderate leuoko’s and neutrophilia
ABX Txm for Appendicitis
Cefoxitin or cefotetan
Ampicillin-Sulbactam
Ertapenem
Normal vascular structures (cushions) in the anal canal, arising from a channel of arteriovenous connective tissues that drains into the superior and inferior hemorrhoidal veins
Hemorrhoids
Internal hemorrhoids
are located proximal to the dentate line
Arise from the superior hemorrhoidal veins
External hemorrhoids
are located distal to the dentate line
Arise from the inferior hemorrhoidal veins
Covered with squamous epithelium of the anal canal or perianal region
Main patio of hemorrhoids
Increased venous pressure
Clinical presentation of hemorrhoids
Most often presenting complaint is bright red rectal bleeding
Streaks on the stool or on the paper —>bright red blood dripping into the toilet
Other symptoms
Perianal itching
Mucoid discharge with stool
Pain —> external hemorrhoids
Prolapse may permit leakage of rectal contents
Patients with leakage may clean aggressively, irritating the perineum and also allowing contact of fecal material with denuded skin
Internal hemorrhoids
Skin tags associated with may be difficult to clean, resulting in prolonged contact of fecal material with the perianal skin and local irritation
External hemorrhoids
What do you inspect for on PE with suspect hemorrhoids
Skin tags, fissures, fistula, condyloma, dermatitis
Anoscopic exam = visualize internal hemorrhoids
Bleeding only no prolapse; GRADE
1
Prolapse with defecation; spontaneous reduction; GRADE
2
Prolapse with defecation: must be manually reduced; GRADE
3
Prolapse with defecation: must be manually reduced; GRADE
3
Prolapsed, incarcerated: cannot be manually reduced; GRADE
4
Thrombosis of the external hemorrhoidal plexus results in
Perianal hematoma
Thrombosed hemorrhoids acute onset =
exquisitely painful
Thrombosis of the external hemorrhoidal plexus results in and bluish perianal nodule covered with skin
Symptoms last 2-3 days, relieved w/warm sitz bath, analgesics, and ointments
Clot excision (clinic) may provide relief if performed w/in 48 hrs
TxM of Hemorrhoids
High fiber diet + increased fluid intake
Avoid straining
Limit sitting time on toilet <5 min
Avoid aggressive wiping
Sitz baths
Med TxM of hemorrhoids
Topical Astringents
Witch hazel pads (Tucks)
Topical Hydrocortisone
Cream or foam (Proctofoam)
Topical anesthetics
Pramoxine or dibucaine
Hydrocortisone suppositories (Preparation H)
Further Txm ; internal hemorrhoids
Rubber band ligation
Sclerotherapy
Electrocoagulation
A tear in the anoderm distal to the dentate line
Anal fissure ; due to trauma of anal canal
Why do chronic anal fissures develop
Spasm of the internal sphincter, with impaired healing
Anal fissures
Examination of the anus reveals small tear in the epithelium
Spreading buttocks may be acutely painful to the patient
Avoid digital rectal examination - pain
May observe “sentinel pile”
(Skin tag at the outermost edge of the fissure)
Primary anal fissure
Posterior (90%) or anterior midline location (25% postpartum women)
Usually single fissure
Rarely located off midline
Secondary anal fissure
Lateral or atypical position offmidline location
Multiple fissures
Chronic IBD, HIV, syphilis, malignancy, granulomatous disease, psoriasis, previous surgery [associations]
Chronic fissure Txm
Topical vasodilators
Nifedipine, nitroglycerin, or diltiazem
Botulinum toxin injection
Surgical TxM
Fissure to my
Lateral internal sphincerotomy
Anorectal infxn
Anorectal abscess typically originates from an obstructed and infected anal crypt gland
Clinical presentation of perianal abscess
Severe pain in the anorectal region
Constant and not directly associated with defecation
Fever and malaise are common
What do you find on PE of perianal abscess
Digital Rectal Exam!!
Rectal abscesses
Fistulas
Perianal =
Perirectal =
Simple ; ID in clinic
Complex ; ID in OR
What can reduce the rate of fistula formation in perianal abscess?
Oral antibiotics
Fistula formation
An epithelialized track can form connecting the abscess in the anus or rectum with the perirectal skin
Leads to chronic purulent drainage, pruritus, pain
Requires surgical excision
What is the usual etiology of infectious proctitis
Etiology usually STI
Gonorrhea
Syphilis
Chlamydia
Herpes
Condylomata acuminata
Anal warts
May c/o itching, bleeding or pain
May coalesce and obscure the anal opening (usually in immunosuppressed patients)
Must distinguish from cancer
Most common symptoms of carcinoma of the anus
Bleeding, pain, local mass
What study is used to ID carcinoma of the anus and distinguish b/w hemorrhoids
CT or MRI to diagnose
