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WHAT TISSUES MAKE UP THE DIAPHRAGM AND
WHAT ARE THEIR INNERVATIONS?
The thoracic diaphragm is derived from four different embryonic tissues:
Septum Transversum: forms central tendon, innervation provided by branches
of the C3-C5 ventral rami (phrenic nerve)
Pleuroperitoneal membranes: form the dorsal aspects of the diaphragm also
innervated by phrenic nerve
Esophageal Mesentery: forms the crura of the diaphragm innervated by the
phrenic nerve
Lateral Body Wall: forms the outermost ring of the diaphragm, sensory
innervation provided by the lower intercostal nerves [intercostal (T5-T11) and
subcostal nerve (T12)]
WHAT COMPLICATION CAN RESULT FROM A
DIAPHRAGMATIC HERNIA? Pulmonary Hypoplasia
WHAT STIMULATES RELEASE OF CCK
Presence of fats and amino acids in the duodenum
WHERE IS MEISSNER’S PLEXUS LOCATED?
Submucosa
Aurbach’s is in the muscularis
IN WHICH PART OF THE BRAIN IS THE VOMITING
CENTER?
Medulla
Reverse peristalsis from LES to UES
Retch occurs if UES does not open
WHAT IS UNIQUE ABOUT SALIVARY BLOOD
FLOW?
The salivary glands have an unusually high blood flow that increases when
saliva production is stimulated. When corrected for organ size, maximal blood
flow to the salivary glands is more than 10 times the blood flow to exercising
skeletal muscle!
WHICH NERVOUS SYSTEM INCREASES
INTESTINAL ABSORPTION? Sympathetic
WHAT IS THE SECOND MESSENGER FOR ACH IN
THE STOMACH?
IP3/Ca2+
WHICH STRUCTURE IS AT RISK WHEN SHARP
OBJECTS BECOME LODGED IN THE PIRIFORM
RECRESS?
Superior Laryngeal Nerve
IS SALIVA HYPOTONIC, ISOTONIC OR
HYPERTONIC AS COMPARED TO THE PLASMA?
When compared with plasma, saliva is hypotonic.
(i.e., has a lower osmolarity), has higher K+ and HCO3 concentrations, and
has lower Na and Cl concentrations. Saliva is formed in a two-step process that
involves several transport mechanisms.
The first step is the formation of an isotonic plasma-like solution by the acinar
cells.
The second step is modification of this plasma-like solution by the ductal cells.
Because more NaCl is absorbed than KHCO3 is secreted, there is net
absorption of solute.
IMPERMEABILITY TO WATER MAINTAINS HYPOTONICITY
ARE PANCREATIC SECRETIONS HYPOTONIC,
ISOTONIC, OR HYPERTONIC?
Isotonic
Na and K+ are the same as in the plasma
CL- and HCO3- vary with flow rate
HCO3- is highest with high flow rate
DURING THE ORAL PHASE OF SWALLOWING,
CONTACT WITH WHICH STRUCTURE INITIATES
THE PHARYNGEAL PHASE?
Palatoglossal Arch
WHAT ARE THE BOUNDARIES OF THE ORAL
VESTIBULE
The dental arches (complete structure associated with the dentition) divide the
oral cavity into two parts: the vestibule and the oral cavity proper
The vestibule of the oral cavity is the U-shaped region found between the
mucous membranes covering the lips and cheeks and the dental arches, gums,
and teeth.
The vestibule communicates with the external environment by means of the
rima oris, the elongated opening or fissure between the lips
. The vestibule communicates with the oral cavity proper by means of the
spaces between the occlusal surfaces of the teeth as well as the space
between the last molar and the pterygomandibular fold.
WHAT ARE THE BOUNDARIES OF THE ORAL
CAVITY PROPER
The dental arches (complete structure associated with the dentition) divide the
oral cavity into two parts: the vestibule and the oral cavity proper. The vestibule
of the oral cavity is the U-shaped region found between the mucous
membranes covering the lips and cheeks and the dental arches, gums, and
teeth. The vestibule communicates with the external environment by means of
the rima oris, the elongated opening or fissure between the lips. The vestibule
communicates with the oral cavity proper by means of the spaces between the
occlusal surfaces of the teeth as well as the space between the last molar and
the pterygomandibular fold.
IN WHICH LAYER ARE THE ESOPHAGEAL
MUCUS SECRETING GLANDS? Submucosa
WHAT SORT OF ORGANELLES ARE
CONCENTRATED IN THE EOSINOPHILIC DUCT
CELLS OF THE SALIVARY GLANDS
Mitochondria
WHY DOES THE PANCREAS APPEAR MORE LIKE
THE PAROTID GLAND THAN THE
SUBMANDIBULAR?
No mucous secreting cells
WHAT TYPE OF CELLS LINE THE BILE DUCT?
Simple columnar
ARE THERE ANY SUBMUCOSAL GLANDS IN THE
STOMACH?
No.
ARE THERE BLOOD VESSELS IN THE GI MUCOSA
Yes the lamina propria has blood vessels.
WHY ARE THE GRANULES IN THE
ENTEROENDOCRINE CELLS SO MUCH SMALLER
THAN THOSE IN THE PANETH CELLS?
Hormones are active at very low concentrations and their signal is amplified by
signaling processes in the cells that have the receptors and hence only small
amounts are needed. This also allows for good temporal resolution. The
products of exocrine secretory cells (like the Paneth cells secreting antibacterial
agents or the pancreatic cells secreting digestive enzymes) are needed in
much larger amounts.]
IS MALT LOCATED IN THE MUCOSA,
SUBMUCOSA, OR BOTH WITHIN THE ILEUM?
Both – use muscularis propria to determine
WHERE ARE GASTRIC STEM CELLS LOCATED
Necks of the gastric glands
Between the glands and gastric pits
WHAT IS THE FUNCTION OF BRUNER’S
GLANDS? The proximal part of the duodenum has in the submucosa and mucosa large
clusters of branched tubular mucous glands, the duodenal (or Brunner) glands,
with small excretory ducts opening among the intestinal crypts.
Mucus from these glands is distinctly alkaline (pH 8.1-9.3), which neutralizes
chyme entering the duodenum from the pylorus, protecting the mucous
membrane, and bringing the intestinal contents to the optimum pH for
pancreatic enzyme action
WHAT SUBSTANCE AT THE MICROVILLAR
SURFACE ANCHORS THE DIGESTIVE ENZYMES
Glycocalyx
IS THE ILEOCECAL SPHINCTER ANATOMICAL OR
PHYSIOLOGICAL? Physiological
Pyloric = anatomical
LES - physiological
HOW DOES THE FETAL ESOPHAGUS DIFFER
FROM THE MATURE ESOPHAGUS?
It is ciliated
WHAT NEUROTRANSMITTER BINDS TO IPANS
TO INITIATE PERISTALSIS?
Serotonin
HOW MUCH FLUID IS SECRETED AND HOW
MUCH FLUID IS LOST IN STOOL DAILY
Approximately 8.5L flows through intestine daily and only 100-200 ml is lost in
stool.
TIGHT JUNCTIONS ARE LEAKY IN THE
AND TIGHT IN THE .
Duodenum
Colon
NET SECRETION AND ABSORPTION
WHAT ARE THE PRESSURES AT THE UES AND
LES RESPECTIVELY?
UES – 50mmHg
LES – 20mmHg
WHERE IS BILE PRODUCED IN THE
HEPATOCYTE?
Smooth ER
COMPARE THE RATE OF SLOW WAVES IN THE
STOMACH TO THE DUODENUM
Stomach – 3/min
Duodenum – 12/min
IS H. PYLORI GRAM NEGATIVE OR GRAM
POSITIVE?
Gram Negative
WHAT CELLS CAN TAKE OVER THE ROLE OF THE
SPLEEN PHAGOCYTOSIS OF RBCS AFTER
SPLENECTOMY?
Kuppfer Cells
HOW DOES FRUCTOSE ENTER THE
ENTEROCYTES?
Facilitated diffusion across the GLUT 5 transporter
IN WHAT PART OF THE SMALL INTESTINE IS
BICARBONATE ABSORBED
Jejunum
HYPERCHLOREMIC METABOLIC ACIDOSIS
Secretory Diarrhea
Cholera
WHAT TWO CONGENITAL GI PATHOLOGIES ARE
ASSOCIATED WITH POLYHYDRAMNIOS?
Esophageal Atresia
Intestinal Atresia
TEF IS ASSOCIATED WITH WHAT SYNDROME?
VACTERL
Vertebral anomalies
Anal atresia
Cardiac defects
TEF
Esophageal atresia
Radial/renal anomalies
Limb defects
NAME TWO GI CONGENITAL DEFECTS
ASSOCIATED WITH DOWN SYNDROME
Duodenal Atresia – DOUBLE BUBBLE
Hirschsprung Disease
WHAT CELL TYPE DOES CMV NOT AFFECT?
SQUAMOUS EPITHELIUM
WHAT ARE THE THREE CARDINAL SIGNS OF
PLUMMER VINSON SYNDROME?
Glossitis
Esophageal webs
Iron deficiency anemia
OTHER SYMPTOMS OF SCLERODERMA
Telangiectasias
Raynaud’s Syndrome
Calcinosis
Collagen deposition
Sclerodactyly
NAME TWO ASSOCIATIONS OF SCHATSKI’S
RINGS
Hiatal Hernia
GERD
IN NUTCRACKER ESOPHAGUS THE
MUSCLE CONTRACTS BEFORE THE
MUSCLE
Longitudinal, circular
SMOOTH MUSCLE ATROPHY AND GUT WALL
FIBROSIS LEADING TO ESOPHAGEAL
APERISTALSIS AND INCOMPETENT LES
Scleroderma Esophagus
ESOPHAGEAL VARICES IN THE ABSENCE OF
PORTAL HYPERTENSION MAY BE CAUSED BY…?
Splenic Vein Thrombosis
Rx: beta blockers, banding, ballone tamponade
NAME ONE OF THE TWO GREATEST RISK
FACTORS FOR BOERHAVE SYNDROME
Alcohol
Duodenal ulcers
WHICH STAIN IS BEST TO VISUALIZE CANDIDA?
Gomori Silver Stain
WHAT IS THE TREATMENT FOR ESOPHAGEAL
HSV IN IMMUNE COMPETENT PATIENTS?
Supportive care
WHAT IS THE SURGERY FOR GERD?
Nissen Fundoplication
WHAT ARE THE TWO TYPES OF HIATAL
HERNIAS?
Sliding hernia (95%) refers to upward displacement of the GE junction and
gastric cardia through the diaphragm
Paraesophgeal hernia (5%) occurs when part of the stomach herniates through
the diaphragm and lies beside the esophagus, without displacement of the GE
junction.
Typically associated with prior thoracic or abdominal surgical procedure
WHAT ARE THE TWO STEPS FOR DIAGNOSIS OF
EOSINOPHILIC ESOPHAGITIS
Endoscopy + Biopsy – must include gastric and duodenal samples
>15 Eos/hpf
Rule out GERD with PPI Trial
WHAT IS A STRUCTURAL FEATURE OF THE
ESOPHAGUS THAT MAKES CANCER
PARTICULARLY DANGEROUS?
No Serosa
WHAT ARE THE RISK FACTORS OF SCC OF THE
ESOPHAGUS?
Risk factors include smoking, alcohol, poverty, caustic esophageal injury,
Plummer-Vinson syndrome, achalasia and mediastinal radiation
Male>>female, black>>>white
Progresses through pathways of squamous dysplasia to carcinoma
WHICH HAS THE WORSE PROGNOSIS IN THE
ESOPHAGUS– SCC OR ADENOCARCINOMA?
Squamous Cell Carcinoma
PYLORIC STENOSIS HAS WHAT TWO MAJOR
ASSOCIATIONS?
Trisomy 18
Turner Syndrome
WHAT CAN BE PALPATED IN PYLORIC
STENOSIS?
An olive shaped mass in the abdomen
NAME TWO MEDICATIONS USED IN
GASTROPARESIS TO INCREASE MOTILITY
Metoclopromide
Erythromycin
Side Effects
Metoclopromide – DOPAMINE ANTAGONIST
Hyperprolactinemia due to inhibition of dopamine receptors - (breast enlargement, galactorrhea, menstrual irregularity)
Tardive dyskinesia symptoms may not reverse easily when the drug is withdrawn.
Parkinson-like symptoms
Erythromycin – Motilin agonist
Drug interactions
Prolonged QT interval
WHAT IS THE DIFFERENCE BETWEEN GASTRITIS
AND GASTROPATHY?
Gastritis is predominantly an inflammatory process while gastropathy
demonstrates minimal to no inflammation as epithelial cell injury and
regeneration are not always accompanied by mucosal inflammation.
Gastritis is commonly secondary to infectious or autoimmune etiologies,
although it can also result from drugs, hypersensitivity reactions, or extreme
stress reactions.
Gastropathy is commonly secondary to endogenous or exogenous irritants,
such as bile reflux, alcohol, or aspirin and nonsteroidal antiinflammatory drugs.
However, gastropathy can also be secondary to ischemia, stress, or chronic
congestion.
WHAT EFFECT CAN A SEVERE BURN OR
TRAUMA HAVE ON THE STOMACH?
Severe burn or trauma causes curling ulcer in proximal duodenum: decreased
plasma volume
WHAT IS THE MOST COMMON GI EMERGENCY?
Upper GI Bleed
HOW DOES H. PYLORI EXERT ITS EFFECTS?
The bacterium generally does not invade gastroduodenal tissue. Instead, it
renders the underlying mucosa more vulnerable to acid peptic damage by
disrupting the mucous layer, liberating enzymes and toxins, and adhering to the
gastric epithelium. In addition, the host immune response to H. pylori incites an
inflammatory reaction which further perpetuates tissue injury.
The chronic inflammation induced by H. pylori upsets gastric acid secretory
physiology to varying degrees and leads to chronic gastritis which, in most
individuals is asymptomatic and does not progress (picture 1A-B). In some
cases, however, altered gastric secretion coupled with tissue injury leads to
peptic ulcer disease, while in other cases, gastritis progresses to atrophy,
intestinal metaplasia, and eventually gastric carcinoma or rarely, due to
persistent immune stimulation of gastric lymphoid tissue, gastric lymphoma
WOMAN WITH HYPOCHLORHYDRIA,
HYPERGASTRINEMIA AND PERNICIOUS ANEMIA
Chronic Autoimmune Gastritis
WHAT TWO TESTS FOR UREASE CAN YOU
PERFORM TO DIAGNOSE H. PYLORI
Urease Breath Test
CLO test on biopsy – will turn red in the presence of urease
DESCRIBE THE MECHANISMS OF DUODENAL
AND GASTRIC ULCERS IN H. PYLORI PUD
Duodenal ulcers probably arise from increased gastric acid being produced
from a normal stomach body as a result of H. Pylori infecting the antrum. It is
also hypothesized that this increased gastric acid may cause small islands of
gastric metaplasia in the duodenal bulb that are then infected with H. Pylori,
leading to duodenitis and ulceration.
Gastric ulcers may occur from a different mechanism. These patients with GUs
have a predominant infection throughout the gastric body that causes
decreased acid production; the infection causes inflammation that overwhelms
the mucosal defense system.
NAME A CARDINAL SYMPTOM AND A CARDINAL
SIGN OF MENETRIER DISEASE?
Peripheral edema due to protein loss (also weight loss, diarrhea, and epigastric
pain)
Cerebriform folds of mucosa
NAME A PARANEOPLASTIC MANIFESTATION OF
GASTRIC TUMORS
Sign of Leser-Trelat – seborrheic keratoses
Acanthosis nigricans
See Approach to upper GI
25% OF ZOLLINGER ELLISON GASTRINOMAS
ARISE IN PATIENTS WITH
MEN1
Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant
predisposition to tumors of the parathyroid glands (which occur in nearly all
patients by age 50 years), anterior pituitary, and entero-pancreatic endocrine
cells
Increased calcium is a cardinal sign
COMPARE AND CONTRAST THE SYMPTOMS OF
GASTRIC AND DUODENAL ULCERS
Gastric: pain in abdomen soon after eating, may not be relieved by antacids
Duodenal: burning, aching pain in upper middle abdomen, 2-3 hrs after eating
or on empty stomach & between 11pm -2am when acid secretion is greatest;
classically, eating can ease pain as bicarb is secreted during cephalic phase
(lecture)
DOES DIFFUSE OR INTESTINAL GASTRIC
CANCER HAVE A WORSE PROGNOSIS?
Diffuse
NAME TWO TESTS FOR H. PYLORI THAT CAN
CONFIRM ERADICATION
Urease breath test
Biopsy
Stool antigen
SERUM ANTIBODY CANNOT
WHICH GASTRIC POLYP IS ASSOCIATED WITH
PPI USE?
Fundic Gland Polyp
Benign
WHICH GASTRIC POLYP IS ASSOCIATED WITH
CHRONIC GASTRITIS?
Hyperplastic Polyp
Benign
NAME 2 PHYSICAL EXAM FINDINGS FOR A
GASTRIC ADENOCARCINOMA
Virchow’s node
Sister Mary Joseph Node
WHAT IS THE COMMON MUTATION OF DIFFUSE
TYPE GASTRIC ADENOCARCINOMA?
CDH1
Diffuse type shows an infiltrative growth pattern throughout the wall of the stomach, often without an obvious surface lesion
The diffuse thickening of the stomach gives in a “leather bottle” appearance termed linitis plastica
Diffuse type infiltrates with “signet ring cell”
Marked desmoplastic response is cause of the rigid, thickened e wall
Often no associated mucosal dysplasia and cancer seems to “drop off” of stomach epithelium
Poorly differentiated
DESCRIBE THE MOST COMMON HISTOLOGICAL
APPEARANCE OF A KRUKENBERG TUMOR.
Signet Ring carcinoma
WHAT IS THE BEST INITIAL TREATMENT FOR
MALT LYMPHOMA IN THE STOMACH?
Antibiotics
Triple therapy
WHAT IS THE BEST THERAPY FOR GIST?
Gleevac
WHAT ASSOCIATION MAKES A GASTRIC
CARCINOID TUMOR PROGNOSIS MORE
FAVORABLE?
Atrophic Gastritis
WHAT ARE SIDE EFFECTS OF MAGNESIUM AND
ALUMINUM Magnesium: Diarrhea
Aluminum: Constipation
WHY IS NOCTURNAL ADMINISTRATION
IMPORTANT FOR H2AS?
Because other stimuli also affect acid secretion, H2As have their greatest effect
on BASAL SECRETION and are more effective with nocturnal administration.
MISOPROSTIL SHOULD NOT BE USED IN THIS
TYPE OF PATIENT
Women who are pregnant or capable of becoming pregnant
Stimulates uterine contractions
Used in medical abortions
WHAT IS THE HALF LIFE OF OMEPRAZOLE AND
HOW LONG DO ITS EFFECTS LAST?
T1/2 = 1 hour
Acid secretion is inhibited for 8-24 hours
OMEPRAZOLE SHOULD NOT BE USED IN
CONJUNCTION WITH…
Plavix – Clopidogrel
Use Pantoprazole instead
WHICH COMPOUND IN ANTACIDS CAN LEAD TO
MILK ALKALI SYNDROME?
CaCO3
CHOLESTYRAMINE AGGRAVATES DIARRHEA IN
PATIENTS WITH…
Extensive Ileal resection
Bile salt depletion
Indicated for Bile salt secretory diarrhea
THESE TWO MEDICATIONS IMPROVE SX OF
CONSTIPATION WITHOUT COMPROMISING
ANALGESIA
Alvimopan
Methylnatrexone
THIS LAXATIVE TARGETS PAIN AND
CONSTIPATION
Linaclotide
ODANSETRON IS A ANTAGONIST
AND BLOCKS SX OF .
5HT-3
Nausea and Vomiting
WHY IS DOMPERIDONE NOT USED IN THE U.S.?
Increased risk of cardiac arrythmias
TWO SIDE EFFECTS OF BISMUTH
Black tongue
Black stools
Tinnitus
WHAT DRUG CAN CAUSE GUM HYPERPLASIA
AND SEVERE NEPHROTOXICITY?
Cyclosporine
WHICH TWO TESTS SHOULD BE PERFORMED
ON A BIOPSY WITH SUSPECTED WHIPPLE
DISEASE
PAS first
If positive, then Acid fast to rule out Mycobacterium
METHOTREXATE SHOULD NOT BE
ADMINISTERED WITH WHAT DRUG?
Cipro
WHAT ARE THE GI ALARM SYMPTOMS?
Alarm symptoms can include fever, dysphagia, odynophagia, GI bleeding, iron
deficiency anemia, and unintentional weight loss. A family history of GI disease
such as colon cancer or inflammatory bowel disease may also be classified as
an alarm symptom.
THESE STRUCTURES CAN CROSS THE
DUODENUM AND CAUSE COMPRESSION OR
OBSTRUCTION IN MALROTATION
Ladd’s Bands
DUODENAL ATRESIA USUALLY RESULTS FROM
FAILURE OF RECANALIZATION WHILE OTHER
INTESTINAL ATRESIAS OFTEN ARISE FROM…
Vascular compromise
May be a result of intrauterine volvulus, intussusception or vascular thrombosis
LOOK FOR DOUBLE BUBBLE
SIGNS OF ACTIVE INFLAMMATION
Neutrophils
Crypt abscesses
Cryptitis
WHAT IS USED TO DIAGNOSE A MECKEL
DIVERTICULUM?
Meckel Scan – radionucleotide study with high sensitivity for gastric epithelium
Rule of twos
2% of population
o 2 feet from ileocecal valve (in adult bowel)
o 2% are symptomatic which typically presents before age of 2
WHAT IS THE GOLD STANDARD FOR DX OF
HIRSCHSPRUNG DISEASE
Rectal Biopsy
WHAT IS THE DEFINITION OF DIARRHEA?
Stool output >200gm/day
Increased frequency
Decreased consistency
PAIN, CRAMPING, DISTENSION, INABILITY TO
PASS GAS, HIGH PITCHED BOWEL SOUNDS
Intestinal Obstruction
WHAT IS AN IMPORTANT CAUSE OF
INTUSSUSCEPTION?
Neoplasm
Kids: enlarged lymph nodes
IN A POSTOP PATIENT WITH PSEUDO-
OBSTRUCTION, WHAT DRUG CAN BE USED IF
CONSERVATIVE RX FAILS?
Neostigmine
PAIN OUT OF PROPORTION TO PHYSICAL
EXAM?
Mesenteric Ischemia
Necrosis of only mucosa and submucosa often due to global hypoperfusion
such as present in shock; may be reversible
Watershed areas at splenic flexure, sigmoid colon and rectum
Transmural (gangrenous) necrosis is usually limited to small intestine,
nonreversible
Thrombosis, or embolism of superior mesenteric artery, usually a result of
atherosclerosis
Mesenteric vein occlusion as seen in cardiac failure, polycythemia vera (red
blood cell disorder) or hypercoaguable states
Mechanical obstruction: volvulus, adhesions, intussusception,strangulated
hernia
HOW SHOULD A DIAGNOSIS OF IBS BE MADE?
HPI
Rome criteria
DO NOT OVERTEST
SIGNS OF MALABSORPTION
Weight loss
Osteomalacia
Increased prothrombin time
Peripheral edema
Steatorrhea
Low albumin
WHAT IS THE DIAGNOSTIC TEST FOR LACTOSE
INTOLERANCE
Hydrogen Breath Test
WHAT CAN YOU TEST FOR CELIAC’S IN A
PATIENT WHO HAS BEEN ON A GLUTEN FREE
DIET?
HLA-DQ2/8
WHAT MALIGNANCY IS ASSOCIATED WITH
CELIAC’S DISEASE
T cell Lymphoma
WHAT ARE THE FOUR CARDINAL SYMPTOMS OF
WHIPPLE DISEASE
Arthralgia
Weight Loss
Diarrhea
Abdominal Pain
Also cardiac, pulmonary and CNS effects
CNS ISSUES!
WHAT ANTIBIOTIC SHOULD YOU GIVE FOR
WHIPPLE DISEASE?
Initial IV antibiotic that can cross BBB: Ceftriaxone
12 mo oral maintenance on Bactrim
WHAT TWO KEY LAB RESULTS CAN YOU SEE
WITH SIBO?
B12 Deficiency
Increased Folate due to synthesis from bacteria
HOW CAN YOU DIAGNOSE SIBO?
Jejunal Aspirate is gold standard, but a D-xylose breath test can be indicative
NAME THREE CONDITIONS WHERE THE PATIENT
SHOULD BE NPO
Diverticulitis
Acute Pancreatitis
Cholecystitis
NAME TWO ABX THAT CAN BE USED FOR SIBO.
Doxycycline, Rifaximin, Amoxicillin-clavulanate
WHICH PART OF THE GI TRACT DO VIRUSES
PRIMARILY ATTACK
Small Intestine
GIARDIA IS MOST OFTEN SEEN ON A BIOPSY OF
WHAT?
Duodenal Biopsy
Seen in spaces between duodenal villi
WHAT DO E. HISTOLYTICA TROPHOZOITES
INGEST THAT CAN BE SEEN ON BIOPSY TO
DISTINGUISH FROM MACROPHAGES
Red Blood Cells
THIS POLYMORPHISM IS ASSOCIATED WITH
CROHN’S DISEASE
NOD2
WHAT INDUCTION DRUG IS USED FOR UC BUT
NOT FOR CROHN’S
Sulfasalazine
CROHN’S DISEASE IS ASSOCIATED WITH THESE
TYPES OF T CELLS
TH1 and TH17
UC is TH1 and TH2
WHAT IS THE BEST METHOD OF
ADMINISTRATION FOR SULFASALAZINE?
Enema
NAME 3 IMPORTANT SIDE EFFECTS OF
GLUCOCORITCOIDS
Suppressed immune response
Cataracts
Osteoporosis
NAME 2 EXTRAINTESTINAL MANIFESTATIONS
OF IBD
Extraintestinal manifestations are common and include:
Seronegative arthritis
Ankylosing spondylitis
Skin rashes (erythema nodosum, pyoderma gangrenosum),
Uveitis (inflammation of iris)
Episcleritis
Thromboembolic events,
Nephrolithiasis
Osteoporosis
SKIP LESIONS, COBBLESTONE MUCOSA,
CREEPING FAT
Crohn’s
WHICH DRUG MUST NOT BE ADMINISTERED
WITH AZATHIOPRINE OR 6-MP
Allopurinol
WHAT IS THE MOST IMPORTANT ADVERSE
EFFECT OF TACROLIMUS AND CYCLOSPORINE
Renal Dysfunction
SERIOUS RISK OF PML
Natalizumab
NAME THE 3 HALLMARK SIGNS OF CHRONIC
MUCOSAL INJURY
Paneth Cell Metaplasia
Basal Plasmacytosis
Distortion of architecture
Crypt forking
WHY IS AZATHIOPRINE USED PRIMARILY AS A
MAINTENANCE DRUG FOR IBD
Delayed onset of action – takes 3-4 months to become therapeutic
Side effects – acute pancreatitis, hepatotoxicity, bone marrow toxicity
WHAT KIND OF MONOCLONAL ANTIBODY IS
INFLIXIMAB?
Chimeric
Part mouse-part human
WHAT TEST MUST BE ADMINISTERED PRIOR TO
STARTING A PATIENT ON A TNF INHIBITOR
PPD TB test
DOES UC OR CROHN’S HAVE A HIGHER RISK OF
SUBSEQUENT NEOPLASIA?
UC
WHAT IS AN IMPORTANT CARDIAC SYMPTOM
OF CARCINOID SYNDROME?
Cardiac Valvular Fibrosis caused by Serotonin
WILL THE FECAL OSMOLAR GAP BE ELEVATED
IN CHOLERA?
No this is a secretory diarrhea
WHAT IS THE MAIN ANTIBIOTIC GIVEN FOR
CHOLERA?
Doxycyclin
Or azithromycin
ABUSE OF WHAT DRUGS CAN LEAD TO
OSMOTIC DIARRHEA?
Laxatives
MIDDLE AGED FEMALE WITH CHRONIC WATERY
DIARRHEA TAKING SERTRALINE
Collagenous Colitis
Rx: stop medications, loperamide, budesonide
DIFFERENTIAL FOR SECRETORY DIARRHEA
Cholera
ETEC
Collagenous Colitis
Lymphocytic colitis
Bile salt diarrhea
Neuroendocrine tumor
Laxative abuse
INFLAMMATORY DIARRHEA DIFFERENTIAL
Salmonella, Shigella, Campylobacter, C diff, Yersinia, Radiation, IBD, E.
Histolytica
WHAT IS THE KEY IMAGING MODALITY FOR
DIAGNOSIS OF DIVERTICULITIS
CT
CT features of acute diverticulitis include:
Increased soft tissue density within pericolic fat, secondary to inflammation –
98 percent
Colonic diverticula – 84 percent
Bowel wall thickening – 70 percent
Soft tissue masses representing phlegmons, and pericolic fluid collections,
representing abscesses – 35 percent
CT can also identify the major complications of diverticulitis, including
peritonitis (with free air, diffuse inflammatory changes, and scattered
loculated fluid collections), fistula formation (usually inferred from
extraluminal air collections in the bladder, vagina, and abdominal wall, rather
than direct visualization), and obstruction.
WHAT ANTIBIOTICS ARE INDICATED FOR
UNCOMPLICATED DIVERTICULITIS?
Reasonable outpatient antibiotic regimens include:
amoxicillin and clavulanate potassium (875 mg/125 mg) twice daily;
OR
metronidazole, 500 mg three times daily; plus either ciprofloxacin, 500 mg
twice daily, or trimethoprim-sulfamethoxazole, 160/800 mg twice daily orally,
for 7–10 days or until the patient is afebrile for 3–5 days.
Patients with severe diverticulitis (high fevers, leukocytosis, or peritoneal signs)
and patients who are elderly or immunosuppressed or who have serious
comorbid disease require hospitalization acutely. Patients should be given
nothing by mouth and should receive intravenous fluids and IV abx.
ELEVATED BUN, NORMAL CREATININE, THINK…
Upper GI bleed
WHAT ARE THE DIAGNOSTIC STUDIES FOR
LOWER GI BLEEDING?
Diagnostic Studies in Acute Lower GI Bleeding (LGIB):
Colonoscopy and sigmoidoscopy: Yield only 40 - 80%, best for slow LGIB—too
much blood obscures view.
Tagged RBC Scan: Nuclear medicine study; often performed prior to
angiography.
Angiography: Contrast injected via arterial catheter. Can embolize a bleeding
vessel.
PRIMARY DIAGNOSTIC TEST FOR
STEATORRHEA?
Fecal Fat: Sudan stain should be first test.
72 hr stool collection is the most reliable and is the gold standard but it requires
high fat diet and prolonged collection.
DIAGNOSTIC TEST FOR INFLAMMATORY
DIARRHEA?
Fecal Leukocytes/Lactoferrin
WHAT IS THE BEST TREATMENT FOR C.
DIFFICILE INFECTION?
Oral Metronidazole or Oral Vancomycin
PSEUDOMONAS COVERAGE
IN A PATIENT WITH SUSPECTED DIVERTICULITIS
WHAT DIAGNOSTIC TEST SHOULD YOU NOT DO?
Colonoscopy – POTENTIAL FOR PERFORATION
GERMLINE MUTATION OF LKB1/STK11 LEADS
TO THIS KIND OF INTESTINAL POLYP
Peutz-Jegher
Christmas tree appearance
Adenocarcinomas arise independently
WHAT IS THE MOST COMMON CANCER
ASSOCIATED WITH PEUTZ JEGHER?
Breast>colon>pancreas
JUVENILE POLYPS ARE ASSOCIATED WITH THIS
MUTATION…
SMAD4
WHAT IS THE MOST COMMON LOCATION FOR A
JUVENILE POLYP?
Rectum
BENIGN HYPERPLASTIC POLYPS MUST BE
DISTINGUISHED FROM THESE MALIGNANT
POLYPS
Sessile Serrated
Crowded colonic glands
Hypermucinous and “sawtooth or starfish”, serrated configurations to surface
and crypts
No cellular dysplastic features.
NAME TWO DYSPLASTIC POLYPS OF THE
INTESTINE AND THEIR GENETIC PATHWAYS
Tubular Adenoma – APC, Wnt
Sessile Serrated - Microsatellite Instability MLH1, MSH2
MOST COMMON IN RIGHT COLON
COLORECTAL CANCER T STAGE CHANGES FROM
1 TO 2 WITH INFILTRATION OF THIS LAYER.
Muscularis
WHAT IS GARDNER SYNDROME?
Gardner syndrome is variant FAP with extragastrointestinal manifestations
o Desmoid tumors (locally aggressive but not metastasizing mesenchymal
tumors), osteomas of jaw (benign)
WHAT COLORECTAL CANCER HAS AN
INCREASED RISKED OF ENDOMETRIAL
CANCER?
HNPCC
WHAT IS THE MOST COMMON LOCATION OF
HNPCC?
Right sided
WHAT ARE THE TWO MAIN MANIFESTATIONS OF
PEUTZ JEGHER?
Mucocutaneous macules
Hamartomatous GI polyps
Muscular stalk
Malignancies arise de novo
WHY IS CARCINOID SYNDROME STRONGLY
ASSOCIATED WITH METASTASIS?
Vasoactive substances are metabolized to inactive forms in the liver
First pass
IN WHICH LOCATION OF THE GI TRACT ARE
CARCINOID TUMORS MOST AGGRESSIVE?
Small intestine
WHAT IS THE TYPICAL APPEARANCE OF A
CARCINOID TUMOR?
Trabecular architecture
Salt and pepper chromatin
WHAT IS PSEUDOMYXOMA PERITONEII?
Clinical condition caused by cancerous cells (mucinous adenocarcinoma) that
produce abundant mucin or gelatinous ascites.
The tumors cause fibrosis of tissues and impede digestion or organ function,
and if left untreated, the tumors and mucin they produce will fill the abdominal
cavity. This will result in compression of organs and will destroy the function of
colon, small intestine, stomach, or other organs.
Prognosis with treatment is good, but the disease is lethal if untreated, with
death by cachexia, bowel obstruction, or other types of complications.
This disease is most commonly caused by an appendiceal primary cancer
WHAT IS THE DOC FOR LISTERIA?
Ampicillin
WHICH ANTIBIOTICS ARE BACTERIOCIDAL
Fluoroquinolones
TMP-SMX – Bactrim
Aminoglycosides
WHICH BACTERIA CAUSES MESENTERIC
LYMPHADENITIS (MIMICS APPENDICITIS)
Yersinia
WHAT IS THE TRIAD OF HUS
Renal Failure
Thrombocytopenia
Hemolytic anemia
WHEN ARE THE INDICATIONS TO SEND A STOOL
CULTURE?
Fever or severe abdominal pain
Diarrhea before vomiting
>3 stools per day
Blood or pus in the stool
WHICH BACTERIA CAN LEAD TO GUILLAIN
BARRE SYNDROME?
Campylobacter jejuni
WHAT AGE IS MOST COMMON FOR INFECTION
BY H. PYLORI
<5 years
WHICH BACTERIA ONLY HAS A HUMAN HOST?
Shigella
WHAT IS THE BEST TREATMENT FOR SHIGELLA?
Azithromycin or Bactrim
Campylobacter can also be treated with azithromycin
WHAT FORM OF GIARDIA IS TRANSMITTED AND
WHAT FORM CAUSES DISEASE?
Cysts are transmitted
Trophozoites cause disease
WHAT IS THE TEST OF CHOICE FOR GIARDIA
Antigen
WHAT IS THE TREATMENT OF CHOICE FOR
CRYPTOSPORIDIUM
Immunocompetent: Nitazoxanide
AIDS: HAART
WHAT ARE THE TWO MAJOR REASONS FOR
FAILURE OF H. PYLORI TREATMENT?
Poor patient compliance
Antibiotic resistance
Clarithromycin, amoxicillin, omeprazole
Metronidazole, tetracycline, bismuth, omeprazole
WHAT ARE THE KAPLAN CRITERIA FOR VIRAL
ETIOLOGY?
Failure to detect bacteria in stool
Vomiting in >50% of patients
Mean illness duration 12-60 hours
Mean incubation 24-48 hours
WHAT ARE THE STRUCTURES AND
CLASSIFICATIONS OF THE MAJOR GI VIRUSES?
Calicivirus: SS RNA + nonenveloped * present in vomit (not seasonal)
Astrovirus: SS RNA + nonenveloped (winter)
Rotavirus: DS RNA segmented nonenveloped (winter) * present in vomit
Adenovirus: DS DNA nonenveloped *survives on surfaces (summer)
THIS PARASITIC INFECTION HAS A HIGH RISK
OF CHOLANGIOCARCINOMA DUE TO
HYPERPLASIA AND FIBROSIS OF THE BILIARY
TRACT
Clonorchis – Liver Fluke
Treat with Praziquantel
DESCRIBE WHAT SUBSTANCES NOROVIRUS
CAN RESIST?
Resistant to chlorine AND alcohol
Must use 1:10 bleach – VERY TRICKY ON CRUISE SHIPS
WHY DOES NOROVIRUS USUALLY ONLY LAST 24
HOURS?
Can only infect mature enterocytes and epithelial turn over eliminates mature
enterocytes in that time period.
WHAT IS A SEAGULL SHAPED BACTERIA
Campylobacter Jejuni
HOW DOES CHOLERA TOXIN EXERT ITS
EFFECTS?
Ribosylates Gs causing activation of adenylate cyclase and increase in cAMP
This leads to the opening of the CFTR channel causing secretion of Cl and Na
and water.
WHICH ORGANISM AND SPECIFIC TOXIN ARE
ASSOCIATED WITH FRIED RICE?
Bacillus Cereus
Heat Stable toxin
WHAT ARE THE INDICATIONS FOR ANTIBIOTIC
TREATMENT IN A CASE OF SALMONELLA?
Severely toxic patient with dysentery or bacteremia
Immunosuppressed
AIDS and receiving immunosuppressing drugs
Infants younger than 3 months
Patients with hemoglobinopathy or asplenia
DOC – Cipro or Azithro or Ceftriaxone with Typhoid fever
WHAT IS THE DOC FOR C. DIFFICILE
Oral metronidazole
Oral vancomycin
WHAT IS THE NAME OF THE THIN LAYER OF
CONNECTIVE TISSUE THAT COVERS THE LIVER?
Glisson’s capsule
TWO IMPORTANT ENZYMES IN THE LIVER FOR
DRUG METABOLISM ARE…
Cytochrome p450
Glucouronyl Transerase
DESCRIBE THE GRADIENT AND KEY
DIFFERENCES BETWEEN ZONE I AND ZONE III
IN THE LIVER
Substances like oxygen and nutrients coming in with the blood are highest in
zone I (perilobular region) and thus metabolic activity requiring oxygen is
highest in this zone (fatty acid oxidation, gluconeogenesis, bile production).
Processes requiring lower oxygen tension occur predominantly in the
centrolobular zone III (glycolysis, fatty acid synthesis).
Zone I is more likely to be damaged by toxic insults, while zone III is most
vulnerable to hypoxic damage.
WHICH CELLS IN THE LIVER ARE CRUCIAL FOR
REGENERATION IN FIBROSIS AND CIRRHOSIS?
Ito (Stellate) cells
DISCUSS THE ROLE OF INSULIN RESISTANCE IN
NAFLD.
Insulin resistances decreases glycogen synthesis and increases breakdown
and gluconeogenesis leading to an abundance of glucose in the hepatocyes
that is used for fatty acid synthesis. Impaired insulin action leads to further
breakdown of glycogen and gluconeogenesis which additionally increases
substrate availabiity.
WHAT EFFECT DOES INSULIN RESISTANCE HAVE
ON VLDL SECRETION
VLDL secretion is increased
Also adipocytes are breaking down fat and unable to uptake circulating fats
Large amount of circulating triglycerides
WHAT TYPE OF CELLS MAKE UP THE
INTRALOBULAR DUCTS OF THE PANCREAS
Simple cuboidal to simple columnar
Interlobular are made up of simple columnar cells and are embedded in
connective tissue
ACUTE HEPATITIS HISTOLOGY?
Lobular lymphocytes
Balooning degeneration
CHRONIC HEPATITIS HISTOLOGY?
Periportal lymphocytes Zone 1
Piecemeal necrosis
Acidophil bodies
Fibrosis
ALD AND NAFLD HISTOLOGY?
Steatosis – Zone 3
Neutrophilic infiltrate
Mallory hyaline bodies
Sclerosing hyaline necrosis – fibrosis around central vein
SOLITARY WELL CIRCUMSCRIBED LIVER MASS
WITH HIGH RISK POTENTIAL FOR
INTRATUMORAL HEMORRHAGE
Hepatic adenoma
Caused by birth control or steroids
MOST COMMON BENIGN TUMOR OF THE LIVER?
Hemangioma
WHAT MARKER IS OFTEN ELEVATED IN
HEPATOCELLULAR CARCINOMA
Alpha Fetoprotein
VERY POOR PROGNOSIS
ALT IS FOUND IN THE WHILE AST IS
FOUND IN THE
Liver cytosol
Liver, skeletal and cardiac muscle, brain and kidney
5’ NUCLEOTIDASE IS A MARKER OF…
Disease of Hepatobiliary origin
GAMMA GLUTAMYL TRANSPEPTIDASE (GGT) IS
A MARKER OF …
Can sometimes be used to distinguish bone from biliary Alkaline phosphatase
However it can also be elevated by drugs and alcohol
BILIRUBINURIA IS EVIDENCE OF…
Direct/Conjugated Hyperbilirubinemia
THESE TWO ANTIBODIES ARE HIGHLY
SENSITIVE FOR AUTOIMMUNE HEPATITIS
Anti-smooth muscle antibody (Type 1 adult onset)
Anti-LKM (Type II child onset)
Also ANA and high IgG
INTERFACE HEPATITIS
TREATMENT FOR AUTOIMMUNE HEPATITIS IS?
Prednisone
Can taper to Azathioprine
ASIAN POPULATIONS MAY LACK THIS ENZYME
CAUSING BUILD UP OF TOXINS LEADING TO
FLUSHING AND TACHYCARDIA
ALDH
WHAT ARE THE SYMPTOMS OF HEREDITARY
HEMOCHROMATOSIS?
Bronze Diabetes
Fatigue
Exocrine and endocrine pancreatic dysfunction
Hepatomegaly
Cardiac conduction dysfunction
Joint arthralgais
WHAT ARE THE TWO PRIMARY MUTATIONS OF
HH?
C82Y
H63D
Of the HFE gene on chromosome 6
Transferrin sat >50% is pathognomonic
LIVER DISEASE WITH CONCOMITANT
NEUROPSYCHIATRIC DISEASE IN ADOLESCENTS
Wilson’s
Kaiser-Fleischer rings
Basal ganglia are affected
LAB RESULTS FOR WILSON’S DISEASE
Low ceruloplasmin
High urinary copper
XANTHEMATOUS LESIONS, ELEVATED ALK
PHOS, FLORID DUCT LESIONS, AMA, ANA,
GRANULOMAS
Primary Biliary Cirrhosis
Autoimmune destruction of small intrahepatic ducts
WHAT IS THE TREATMENT FOR PBC?
Urdeoxycholic Acid
UC, PROGRESSIVE JAUNDICE, ONION SKINNING
FIBROSIS, PRURITIS, ANOREXIA
Primary Sclerosing Cholangitis
Autoimmune destruction of of LARGE DUCTS
DX with ERCP (beading)
WATCH OUT FOR CHOLANGIOCARCINOMA!
PAINFUL HEPATIC ENLARGEMENT, JAUNDICE,
SPLENOMEGALY WITH HYPERCOAGULABILITY
OR A PROMINENT CAUDATE LOBE
Budd Chiari
Dx with Doppler Ultrasound
3 EXAMPLES OF AGENTS CAUSING DIRECT
DRUG INDUCED LIVER DISEASE
Acetaminophen (depletes glutathione)
Alcohol
Statins
Tetracyclins
Niacin
Valproic acid
WHAT IS THE ANTIDOTE FOR ACETAMINOPHEN
INDUCED ACUTE LIVER FAILURE?
N-acetylceystein
Amanita phylloides – silbinin
Do not correct INR – should be used to monitor liver status
WHAT ARE THE SYMPTOMS OF PORTAL
HYPERTENSION?
Jaundice
Scleral icterus
Palmar erythema
Spider angiomata
Gynecomastia
Testicular atrophy
Caput medusae
Ascites
Low platelets
asterixis
IF SAAG IS >1.1 SUSPECT…
Portal Hypertension
If protein >2.5 suspect CHF or Budd Chiari
WHAT IS THE TREATMENT FOR ASCITES?
Salt restriction
Spirolactone – potassium sparing
Furosemide
Therapeutic large volume paracentesis
Consider TIPS - but not before getting an ECHO!!
WHAT IS THE UNDERLYING CAUSE OF
SPONTANEOUS BACTERIAL PERITONITIS
Low protein ascitic fluid leads to decreased opsonizing ability
Most common cause of death is renal failure
Dx with >250 PMNs/ml
WHAT IS THE BEST TREATMENT FOR SBP?
Cephalosporin
Prophylactic Cipro or Bactrim
E. Coli is most common (gram + cocci also)
ALSO AMP-SULF
WHAT ARE THREE PRECIPITATING CONDITIONS
FOR HEPATIC ENCEPHALOPATHY
Hypovolemia
Sedatives/narcotics
Infection
Acute GI bleed
Diet
BUT DO NOT EVER ORDER A PROTEIN RESTRICTED DIET
WHAT IS THE TREATMENT FOR HEPATIC
ENCEPHALOPATHY?
Lactulose – acidifies the colon
Rifaximin – eliminates ammonia producing bacteria
DO NOT MONITOR AMMONIA AS A MARKER
NAME TWO PHYSICAL EXAM FINDINGS FOR
HEPATOPULMONARY SYNDROME
Platypnea – greater dyspnea in seated position than recumbent
Orthodeoxia – arterial deoxygenation in seated position
WHAT ARE THE THREE MEASURES OF MELD
INR
Creatinine
Total Bilirubin
HIGH SPIKING FEVER WITH FATIGUE AND RUQ
PAIN AND TENDERNESS TO PALPATION,
VARIABLE JAUNDICE, LEFT SHIFT WBC
LIVER ABSCESS
E. coli
Klebsiella
Proteus
E. aerogenes
Streptococcus
RX: abx., drainage, no surgery unless >5cm
WHAT DIAGNOSTIC TEST IS CONTRAINDICATED
WITH AN AMEBIC ABSCESS?
Biopsy can cause peritoneal spilling and peritonitis
NAME THE BENIGN LIVER LESIONS
Hemangioma
Hepatic adenoma
Focal nodular hyperplasia
WHAT IS THE CHARACTERISTIC FINDING OF A
HEMANGIOMA ON IMAGING?
Peripheral enhancement with delayed central filling
DISCUSS THE IMAGING MODALITY THAT IS BEST
FOR HEPATOCELLULAR CARCINOMA
Triple Phase CT or MRI
High enhancement in the arterial phase (due to vascularity of HCC), and then
“rapid washout” in the next phase (little venous filling) is very specific for HCC.
DO NOT BIOPSY – potential for seeding
NAME THE TWO MOST COMMON MODALITIES
OF TREATMENT FOR HCC
Trans-arterial Chemoembolization
Radiofrequency Ablation
WHAT ARE THE MILAN CRITERIA FOR LIVER
TRANSPLANTATION?
3 HCC lesions less than 3 cm or 1 lesion less than 5cm
WHAT ARE THE FOUR F’S OF CHOLESTEROL
CHOLELITHIASIS?
Female
Fat
Fertile
Forty
WHAT ARE THE INDICATIONS FOR A
CHOLECYSTECTOMY?
Pain
Calcified gallbladder (porcelain)
Stone > 3cm
Polyp > 1 cm
WHAT PROPHYLACTIC MEASURES CAN BE
TAKEN IN A BARIATRIC SURGERY TO REDUCE
FORMATION OF GALLSTONES
Prophylactic cholecystectomy
Ursodeoxycholic acid
WHAT RISKS DOES PORCELAIN GALLBLADDER
HAVE?
50% chance of malignancy
REMOVE!
SEVERE RUQ PAIN, VOMITING, FEVER, +
MURPHY’S SIGN, HIGH WBC (NO JAUNDICE)
Acute Cholecystitis
WHAT IS THE MOST SENSITIVE TEST FOR ACUTE
CHOLECYSTITIS/CYSTIC DUCT BLOCKAGE?
HIDA scan
WHAT IS REYNOLD’S PENTAD?
Indications of ascending cholangitis
Fever
Jaundice
RUQ pain
Altered mental status
Hypotension
WHAT IS THE TREATMENT FOR CHOLANGITIS?
ERCP and Pip-tazo/amp-sulf/mero (life threatening)
Also cip + metro
NAME TWO CONDITIONS THAT INCREASE RISK
FOR CHOLANGIOCARCINOMA
PSC
Choledochal cyst
Diverticulae
Parasitic infections from Asia
Klatskin tumor
Gray nodular infiltrative growth
HOW IS DIAGNOSIS OF A GALLSTONE ILEUS
MADE?
CT or XRAY demonstrating pneumobilia
Surgical removal needed
BORING EPIGASTRIC PAIN RADIATING TO BACK
WITH NAUSEA VOMITING ANOREXIA AND
WORSENING PAIN WITH WALKING OR LYING
Acute Pancreatitis
Elevated lipase
WHAT TWO SIGNS ARE WORRISOME FOR
NECROTIZING PANCREATITIS
Cullen’s sign – bruising around umbilicus
Turner’s sign – flank bruising
WHAT ARE THE TWO MOST COMMON
ETIOLOGIES OF ACUTE PANCREATITIS
Alcohol
Gallstones
WHAT PANCREATIC TUMOR PRESENTS WITH
ORGANOID OR TRABECULAR TUMOR CELLS
AND A WELL CIRCUMSCRIBED MASS
Pancreatic Neuroendocrine Tumor
Insulinoma
Gastrinoma
Many are found incidentally
Non functioning neoplasms (must have clinicial sx)
Very good prognosis
WHAT ARE THE MOST DESMOPLASTIC
TUMORS?
Pancreatic ductal adenocarcinoma
WHAT IS THE STANDARD TREATMENT FOR
ACUTE PANCREATITIS?
NPO
Fluid resuscitation
Pain management
Potential for TPN
NAME THREE COMPLICATIONS OF ACUTE
PANCREATITIS
Pancreatic Ascites
Third spacing – Volume depletion
Acute kidney failure
Shock
ARDS (respiratory failure)
Necrosis/infection/abscess
Pseudcocyst
WHAT IS THE BEST TREATMENT FOR
AUTOIMMUNE PANCREATITIS?
Steroids
WHAT COMPLICATIONS ARE ASSOCIATED WITH
CHRONIC PANCREATITIS
Duodenal Obstruction
Biliary stricture
Pseudocyst
Cancer
HIGH ALK PHOS OR BILI WITHOUT EVIDENCE OF
BILIARY DISEASE….
Infiltrative or metastatic disease!
EPIGASTRIC PAIN, STEATORRHEA, DIABETES
Chronic pancreatitis
ALCOHOL, divisum
Fibrosis and calcification (visible on CT often)
ERCP is best for diagnosis
WHAT IS THE NUMBER ONE CAUSE OF
NEONATAL JAUNDICE?
Biliary atresia
Also the main cause of liver transplants in children
WHAT SHOULD YOU THINK OF WITH A VERY
LOW ALKALINE PHOSPHATASE?
Acute Wilson’s Disease
WHAT IS THE CAUSE OF STRAWBERRY
GALLBLADDER?
Cholesterolosis – cholesterol builds up in macrophages within lamina propria
WHAT IS A CRITICAL STEP IN A
CHOLECYSTECTOMY?
Demonstrate there are no stones in the common bile duct
DESCRIBE THE MECHANISM FOR SALTY SWEAT
IN CYSTIC FIBROSIS
Dysfunctional CFTR in sweat glands means that there will be diminished
chloride reabsorption, resulting in a greater lumen negative transepithelial
potential and thus limited sodium reabsorption → excess salt loss in sweat
Can lead to serious dehydration in hot weather
DESCRIBE THE MECHANISM OF PANCREATIC
INSUFFICIENCY IN CYSTIC FIBROSIS
In the pancreatic ducts the CFTR transporter is necessary for secretion of
Chloride. This secretion is critical for the secretion of HCO3- through the
chloride bicarb exchange. This leads to less fluid secreted, causing plugging of
the ducts and inability to secrete digestive enzymes.
WHAT ARE THE SYMPTOMS OF CYSTIC
FIBROSIS?
Recurrent pulmonary infections
Pancreatic insufficiency
Salty sweat
Nutritional deficits
Night blindness (vitamin A)
Neurologic dysfunction (vitamin E)
Immune and bone effects (vitamin D)
Platelets (vitamin K)
Hyperacidity of duodenum (give PPIs)
DO CF PATIENTS EXPERIENCE OSMOTIC
DIARRHEA OR SECRETORY DIARRHEA?
Secretory Diarrhea – bacteria hydrolyze fats hydroxy fatty acids stimulate
cAMP which leads to secretory diarrhea
WHAT IS THE BEST MANAGEMENT PANCREATIC
INSUFFICIENCY DUE TO CYSTIC FIBROSIS?
Pancreatic enzymes
PPIs
High fat diet
Vitamin supplements
DESCRIBE THE CLINICAL PRESENTATION OF
PYLORIC STENOSIS
Nonbilious projectile vomiting usually between 1-5 weeks of age
Regurgitation
Dehydration
Infant hungry after vomiting
COMPARE THE PREVALENCE OF PYLORIC
STENOSIS BETWEEN MALES AND FEMALES
F – 1/1000
M – 5/1000
NAME THREE OF THE SIX CHARACTERISTICS OF
MULTIFACTORIAL INHERITANCE
1) Although disorder familial, no distinctive pattern of inheritance within family
2) Risk to first degree relatives, determined by family studies, approx. square
root of population risk
3) Risk sharply lower for second degree than first degree, but declines less
rapidly for more remote relatives
4) Recurrence risk higher when more than one family member is affected
5) More severe the malformation (or any phenotype), the greater recurrence
risk
6) If it is more frequent in one sex than the other, the recurrence risk is higher
for relatives of less susceptible sex
DESCRIBE THE MODE OF INHERITANCE OF
HEREDITARY HEMOCHROMATOSIS
Autosomal recessive
WHAT ARE THE RISKS OF 1ST, 2ND, AND 3RD
DEGREE RELATIVES OF CARRIERS?
1st: 1/2
2nd: 1/4
3rd: 1/8
WHAT IS THE BEST TEST FOR DIAGNOSIS OF
HEREDITARY HEMOCHROMATOSIS
Serum transferrin saturation
RX: Phlebotomy 1-2x/week until 25-50mg ferritin/L
PHLEBOTOMY CAN ALLEVIATE MOST OF THE
SYMPTOMS OF HEREDITARY HEMOCHROMATOSIS
EXCEPT…
Arthritis
NAME THREE COPPER RICH FOODS THAT
SHOULD BE AVOIDED IN WILSON’S DISEASE
Nuts
Chocolate
Mushrooms
Shellfish
IN WILSON’S DISEASE DO HEPATIC OR
NEUROLOGIC SYMPTOMS TYPICALLY PRESENT
FIRST?
Hepatic
DESCRIBE THE GENETIC ETIOLOGY OF
WILSON’S DISEASE
Autosomal recessive mutation of ATP7B leads to copper transport dysfunction
and build up of copper in organs
Ceruloplasmin cannot bind copper
Buildup occurs first in liver and then overload leads to spillage into bloodstream
and other organs
BEST DX TEST: liver biopsy
WHAT IS THE BEST TREATMENT FOR CHRONIC
RETENTIVE CONSTIPATION IN PEDIATRIC PTS.?
Oral disimpaction
24 hr liquid diet
Golytely
Behavioral Modification
WHAT PEDIATRIC POPULATIONS ARE AT HIGH
RISK FOR GERD?
Several pediatric populations are at increased risk for the development of
GERD, including patients who have neurologic impairment, obesity, lung
disease (specifically cystic fibrosis), esophageal atresia, and prematurity.
FOOD IMPACTION WITH HISTORY OF ASTHMA,
ATOPIC DERMATITIS OR ALLERGIC RHINITIS
Eosinophilic Esophagitis
WHAT CONSERVATIVE MEASURE OFTEN
ALLEVIATES SYMPTOMS OF EOE
Elimination of allergic foods
WHAT IS A KEY GROSS FINDING OF
LATE/SEVERE EOE?
Trachealization of the esophagus
Strictures
NAME TWO WAYS TO DISTINGUISH BETWEEN
SUPINE AND UPRIGHT RADIOGRAPHS?
Two main ways to distinguish between upright and supine computed
radiography images:
First evaluate the structures that contain air
Supine radiograph: ventral structures (e.g., antrum of the stomach) contain
air
Upright radiograph: superior structures (e.g., fundus of the stomach) contain
air
Then look for air fluid levels
These are horizontal interfaces with air above and fluid below
NAME TWO RADIOLOGICAL FINDINGS FOR
ACUTE PANCREATITIS
Diffuse enlargement with peripancreatic inflammation (fat stranding)
Fluid collection – abscess or pseudocyst
WHAT IS THE BEST WAY TO DISTINGUISH
BETWEEN THE ILEUM AND THE JEJUNUM ON A
RADIOGRAPH?
The plicae circularis give the jejunum a feathery appearance
WHAT ARE THE NORMAL DIAMETERS OF THE
SMALL INTESTINE, TRANSVERSE COLON AND
CECUM
3, 6, 9
WHAT IS THE BEST IMAGING TEST FOR ACUTE
ABDOMEN?
Abdominal series
Only do CT if there are no surgical indications:
Involuntary guarding or rigidity, tenderness
Distention
Abdominal or rectal mass with high fever or hypotension
Bleeding with shock or acidosis
Septicemia
Suspected ischemia
Pneumoperitoneum
Free extravasation of contrast material
Space-occupying lesion on imaging, with fever
WHAT IS THE BEST IMAGING FOR ACUTE
CHOLECYSTITIS?
Ultrasound
WHAT IS THE BEST IMAGING FOR
DIVERTICULITIS?
CT
WHAT ARE THE RADIOLOGICAL FINDINGS OF A
PERFORATED VISCUS?
Free air on AXR
WHAT ARE THE RADIOLOGICAL FINDINGS FOR
SMALL BOWEL OBSTRUCTION?
Dilated small bowel loops
Ladder like air fluid levels
RADIOLOGICAL FINDINGS FOR CECAL AND
SIGMOID VOLVULUS
Coffee bean
Sigmoid : LLQ
Cecal : RLQ
WHAT RADIOLOGICAL SIGN IN THE ILEUM CAN
INDICATE CROHN’S DISEASE?
String sign
Nodularity and ulceration
WHAT SHOULD YOU LOOK FOR ON A CT FOR
SUSPECTED APPENDICITIS?
Distended appendix with hyperenhancement and periappendiceal fat stranding
WHAT IS THE CLASSIC RADIOLOGICAL SIGN OF
COLON CANCER?
Apple core lesion
WHAT ARE THE INDICATIONS FOR
ABDOMINOPERINEAL RESECTION?
Rectal cancer at level of puborectalis muscle/sphincter complex
Crohn's with refractory perianal fistula
Persistent/recurrent anal squamous cell cancer
WHAT ARE THE TWO MOST COMMON
SURGERIES FOR MEDICALLY REFRACTORY
ULCERATIVE COLITIS?
Permanent end ileostomy: the end of the ileum (free after the proctocolectomy)
is brought out to the surface of the skin and the bowel is everted to expose the
mucosa. The end is attached to a bag reservoir which catches the intestinal
contents. The intestinal bud must be kept a few inches off the surface of the
skin so that there is decreased risk of digestive enzymes leaking onto the skin
under the pouch system.
Ileoanal pouch: Serves as an internal reservoir solution to the colectomy. The
ileum is folded back onto itself and stapled together. The walls between the
folds are taken out to create one big pouch reservoir that can connect directly
to the anal sphincter if it is kept intact.
DESCRIBE THE TWO MOST COMMON BARIATRIC
SURGERIES
Gastric banding: The surgery works by taking a band and wrapping it around
the proximal stomach. Creates a reservoir system that allows adjustment of
tightness of the band. The band allows for slow intake of food and induces early
satiety. It is important to remember that the band will have no effect on gastric
emptying.
Gastric Bypass: The first step is to divide the stomach into two sections. the
first section attaches a piece of jejunum (called a Roux limb) directly from the
cardia of the stomach to the duodenum/jejunum (this is the bypass part). The
second section is therefore completely cut off from the esophagus and the
inbound food supply, so it stays empty and serves to deliver bile and other
enzymes when the two sections meet back up in the jejunum.
WHAT ARE TWO INDICATIONS FOR GASTRIC
RESECTION?
PUD
Cancer
Biliroth I: distal gastrectomy + anastomosis of stomach remnant and duodenum
Biliroth II: antrectomy + jejunal loop anastomosis for drainage
DESCRIBE THE DIFFERENCES IN MANAGEMENT
FOR CECAL VS. SIGMOID VOLVULUS
Sigmoid volvulus : endoscopic decompression as long as there are no signs of
strangulation followed by elective sigmoid resection
Cecal volvulus: emergent colectomy
“FEAR OF EATING” – CHRONIC POST PRANDIAL
PAIN AND WEIGHT LOSS
Intestinal angina
Manage atherosclerosis
Stenting
Mesenteric bypass
DIAGNOSIS AND TREATMENT OF
AORTOENTERIC FISTULA?
Endoscopy
Emergent laparotomy
Most common in 3rd and 4th parts of the duodenum