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GI Review

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Page 1: GI Review
Page 2: GI Review
Page 3: GI Review

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)]

Page 4: GI Review

WHAT COMPLICATION CAN RESULT FROM A

DIAPHRAGMATIC HERNIA? Pulmonary Hypoplasia

Page 5: GI Review

WHAT STIMULATES RELEASE OF CCK

Presence of fats and amino acids in the duodenum

Page 6: GI Review

WHERE IS MEISSNER’S PLEXUS LOCATED?

Submucosa

Aurbach’s is in the muscularis

Page 7: GI Review

IN WHICH PART OF THE BRAIN IS THE VOMITING

CENTER?

Medulla

Reverse peristalsis from LES to UES

Retch occurs if UES does not open

Page 8: GI Review

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!

Page 9: GI Review

WHICH NERVOUS SYSTEM INCREASES

INTESTINAL ABSORPTION? Sympathetic

Page 10: GI Review

WHAT IS THE SECOND MESSENGER FOR ACH IN

THE STOMACH?

IP3/Ca2+

Page 11: GI Review

WHICH STRUCTURE IS AT RISK WHEN SHARP

OBJECTS BECOME LODGED IN THE PIRIFORM

RECRESS?

Superior Laryngeal Nerve

Page 12: GI Review

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

Page 13: GI Review

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

Page 14: GI Review

DURING THE ORAL PHASE OF SWALLOWING,

CONTACT WITH WHICH STRUCTURE INITIATES

THE PHARYNGEAL PHASE?

Palatoglossal Arch

Page 15: GI Review

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.

Page 16: GI Review

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.

Page 17: GI Review

IN WHICH LAYER ARE THE ESOPHAGEAL

MUCUS SECRETING GLANDS? Submucosa

Page 18: GI Review

WHAT SORT OF ORGANELLES ARE

CONCENTRATED IN THE EOSINOPHILIC DUCT

CELLS OF THE SALIVARY GLANDS

Mitochondria

Page 19: GI Review

WHY DOES THE PANCREAS APPEAR MORE LIKE

THE PAROTID GLAND THAN THE

SUBMANDIBULAR?

No mucous secreting cells

Page 20: GI Review

WHAT TYPE OF CELLS LINE THE BILE DUCT?

Simple columnar

Page 21: GI Review

ARE THERE ANY SUBMUCOSAL GLANDS IN THE

STOMACH?

No.

Page 22: GI Review

ARE THERE BLOOD VESSELS IN THE GI MUCOSA

Yes the lamina propria has blood vessels.

Page 23: GI Review

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.]

Page 24: GI Review

IS MALT LOCATED IN THE MUCOSA,

SUBMUCOSA, OR BOTH WITHIN THE ILEUM?

Both – use muscularis propria to determine

Page 25: GI Review

WHERE ARE GASTRIC STEM CELLS LOCATED

Necks of the gastric glands

Between the glands and gastric pits

Page 26: GI Review

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

Page 27: GI Review

WHAT SUBSTANCE AT THE MICROVILLAR

SURFACE ANCHORS THE DIGESTIVE ENZYMES

Glycocalyx

Page 28: GI Review

IS THE ILEOCECAL SPHINCTER ANATOMICAL OR

PHYSIOLOGICAL? Physiological

Pyloric = anatomical

LES - physiological

Page 29: GI Review

HOW DOES THE FETAL ESOPHAGUS DIFFER

FROM THE MATURE ESOPHAGUS?

It is ciliated

Page 30: GI Review

WHAT NEUROTRANSMITTER BINDS TO IPANS

TO INITIATE PERISTALSIS?

Serotonin

Page 31: GI Review

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.

Page 32: GI Review

TIGHT JUNCTIONS ARE LEAKY IN THE

AND TIGHT IN THE .

Duodenum

Colon

Page 33: GI Review

NET SECRETION AND ABSORPTION

Page 34: GI Review

WHAT ARE THE PRESSURES AT THE UES AND

LES RESPECTIVELY?

UES – 50mmHg

LES – 20mmHg

Page 35: GI Review

WHERE IS BILE PRODUCED IN THE

HEPATOCYTE?

Smooth ER

Page 36: GI Review

COMPARE THE RATE OF SLOW WAVES IN THE

STOMACH TO THE DUODENUM

Stomach – 3/min

Duodenum – 12/min

Page 37: GI Review

IS H. PYLORI GRAM NEGATIVE OR GRAM

POSITIVE?

Gram Negative

Page 38: GI Review

WHAT CELLS CAN TAKE OVER THE ROLE OF THE

SPLEEN PHAGOCYTOSIS OF RBCS AFTER

SPLENECTOMY?

Kuppfer Cells

Page 39: GI Review

HOW DOES FRUCTOSE ENTER THE

ENTEROCYTES?

Facilitated diffusion across the GLUT 5 transporter

Page 40: GI Review

IN WHAT PART OF THE SMALL INTESTINE IS

BICARBONATE ABSORBED

Jejunum

Page 41: GI Review

HYPERCHLOREMIC METABOLIC ACIDOSIS

Secretory Diarrhea

Cholera

Page 42: GI Review
Page 43: GI Review

WHAT TWO CONGENITAL GI PATHOLOGIES ARE

ASSOCIATED WITH POLYHYDRAMNIOS?

Esophageal Atresia

Intestinal Atresia

Page 44: GI Review

TEF IS ASSOCIATED WITH WHAT SYNDROME?

VACTERL

Vertebral anomalies

Anal atresia

Cardiac defects

TEF

Esophageal atresia

Radial/renal anomalies

Limb defects

Page 45: GI Review

NAME TWO GI CONGENITAL DEFECTS

ASSOCIATED WITH DOWN SYNDROME

Duodenal Atresia – DOUBLE BUBBLE

Hirschsprung Disease

Page 46: GI Review

WHAT CELL TYPE DOES CMV NOT AFFECT?

SQUAMOUS EPITHELIUM

Page 47: GI Review

WHAT ARE THE THREE CARDINAL SIGNS OF

PLUMMER VINSON SYNDROME?

Glossitis

Esophageal webs

Iron deficiency anemia

Page 48: GI Review

OTHER SYMPTOMS OF SCLERODERMA

Telangiectasias

Raynaud’s Syndrome

Calcinosis

Collagen deposition

Sclerodactyly

Page 49: GI Review

NAME TWO ASSOCIATIONS OF SCHATSKI’S

RINGS

Hiatal Hernia

GERD

Page 50: GI Review

IN NUTCRACKER ESOPHAGUS THE

MUSCLE CONTRACTS BEFORE THE

MUSCLE

Longitudinal, circular

Page 51: GI Review

SMOOTH MUSCLE ATROPHY AND GUT WALL

FIBROSIS LEADING TO ESOPHAGEAL

APERISTALSIS AND INCOMPETENT LES

Scleroderma Esophagus

Page 52: GI Review

ESOPHAGEAL VARICES IN THE ABSENCE OF

PORTAL HYPERTENSION MAY BE CAUSED BY…?

Splenic Vein Thrombosis

Rx: beta blockers, banding, ballone tamponade

Page 53: GI Review

NAME ONE OF THE TWO GREATEST RISK

FACTORS FOR BOERHAVE SYNDROME

Alcohol

Duodenal ulcers

Page 54: GI Review

WHICH STAIN IS BEST TO VISUALIZE CANDIDA?

Gomori Silver Stain

Page 55: GI Review

WHAT IS THE TREATMENT FOR ESOPHAGEAL

HSV IN IMMUNE COMPETENT PATIENTS?

Supportive care

Page 56: GI Review

WHAT IS THE SURGERY FOR GERD?

Nissen Fundoplication

Page 57: GI Review

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

Page 58: GI Review

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

Page 59: GI Review

WHAT IS A STRUCTURAL FEATURE OF THE

ESOPHAGUS THAT MAKES CANCER

PARTICULARLY DANGEROUS?

No Serosa

Page 60: GI Review

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

Page 61: GI Review

WHICH HAS THE WORSE PROGNOSIS IN THE

ESOPHAGUS– SCC OR ADENOCARCINOMA?

Squamous Cell Carcinoma

Page 62: GI Review
Page 63: GI Review

PYLORIC STENOSIS HAS WHAT TWO MAJOR

ASSOCIATIONS?

Trisomy 18

Turner Syndrome

Page 64: GI Review

WHAT CAN BE PALPATED IN PYLORIC

STENOSIS?

An olive shaped mass in the abdomen

Page 65: GI Review

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

Page 66: GI Review

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.

Page 67: GI Review

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

Page 68: GI Review

WHAT IS THE MOST COMMON GI EMERGENCY?

Upper GI Bleed

Page 69: GI Review

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

Page 70: GI Review

WOMAN WITH HYPOCHLORHYDRIA,

HYPERGASTRINEMIA AND PERNICIOUS ANEMIA

Chronic Autoimmune Gastritis

Page 71: GI Review

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

Page 72: GI Review

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.

Page 73: GI Review

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

Page 74: GI Review

NAME A PARANEOPLASTIC MANIFESTATION OF

GASTRIC TUMORS

Sign of Leser-Trelat – seborrheic keratoses

Acanthosis nigricans

See Approach to upper GI

Page 75: GI Review

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

Page 76: GI Review

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)

Page 77: GI Review

DOES DIFFUSE OR INTESTINAL GASTRIC

CANCER HAVE A WORSE PROGNOSIS?

Diffuse

Page 78: GI Review

NAME TWO TESTS FOR H. PYLORI THAT CAN

CONFIRM ERADICATION

Urease breath test

Biopsy

Stool antigen

SERUM ANTIBODY CANNOT

Page 79: GI Review

WHICH GASTRIC POLYP IS ASSOCIATED WITH

PPI USE?

Fundic Gland Polyp

Benign

Page 80: GI Review

WHICH GASTRIC POLYP IS ASSOCIATED WITH

CHRONIC GASTRITIS?

Hyperplastic Polyp

Benign

Page 81: GI Review

NAME 2 PHYSICAL EXAM FINDINGS FOR A

GASTRIC ADENOCARCINOMA

Virchow’s node

Sister Mary Joseph Node

Page 82: GI Review

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

Page 83: GI Review

DESCRIBE THE MOST COMMON HISTOLOGICAL

APPEARANCE OF A KRUKENBERG TUMOR.

Signet Ring carcinoma

Page 84: GI Review

WHAT IS THE BEST INITIAL TREATMENT FOR

MALT LYMPHOMA IN THE STOMACH?

Antibiotics

Triple therapy

Page 85: GI Review

WHAT IS THE BEST THERAPY FOR GIST?

Gleevac

Page 86: GI Review

WHAT ASSOCIATION MAKES A GASTRIC

CARCINOID TUMOR PROGNOSIS MORE

FAVORABLE?

Atrophic Gastritis

Page 87: GI Review
Page 88: GI Review

WHAT ARE SIDE EFFECTS OF MAGNESIUM AND

ALUMINUM Magnesium: Diarrhea

Aluminum: Constipation

Page 89: GI Review

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.

Page 90: GI Review

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

Page 91: GI Review

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

Page 92: GI Review

OMEPRAZOLE SHOULD NOT BE USED IN

CONJUNCTION WITH…

Plavix – Clopidogrel

Use Pantoprazole instead

Page 93: GI Review

WHICH COMPOUND IN ANTACIDS CAN LEAD TO

MILK ALKALI SYNDROME?

CaCO3

Page 94: GI Review

CHOLESTYRAMINE AGGRAVATES DIARRHEA IN

PATIENTS WITH…

Extensive Ileal resection

Bile salt depletion

Indicated for Bile salt secretory diarrhea

Page 95: GI Review

THESE TWO MEDICATIONS IMPROVE SX OF

CONSTIPATION WITHOUT COMPROMISING

ANALGESIA

Alvimopan

Methylnatrexone

Page 96: GI Review

THIS LAXATIVE TARGETS PAIN AND

CONSTIPATION

Linaclotide

Page 97: GI Review

ODANSETRON IS A ANTAGONIST

AND BLOCKS SX OF .

5HT-3

Nausea and Vomiting

Page 98: GI Review

WHY IS DOMPERIDONE NOT USED IN THE U.S.?

Increased risk of cardiac arrythmias

Page 99: GI Review

TWO SIDE EFFECTS OF BISMUTH

Black tongue

Black stools

Tinnitus

Page 100: GI Review

WHAT DRUG CAN CAUSE GUM HYPERPLASIA

AND SEVERE NEPHROTOXICITY?

Cyclosporine

Page 101: GI Review

WHICH TWO TESTS SHOULD BE PERFORMED

ON A BIOPSY WITH SUSPECTED WHIPPLE

DISEASE

PAS first

If positive, then Acid fast to rule out Mycobacterium

Page 102: GI Review

METHOTREXATE SHOULD NOT BE

ADMINISTERED WITH WHAT DRUG?

Cipro

Page 103: GI Review
Page 104: GI Review

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.

Page 105: GI Review

THESE STRUCTURES CAN CROSS THE

DUODENUM AND CAUSE COMPRESSION OR

OBSTRUCTION IN MALROTATION

Ladd’s Bands

Page 106: GI Review

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

Page 107: GI Review

SIGNS OF ACTIVE INFLAMMATION

Neutrophils

Crypt abscesses

Cryptitis

Page 108: GI Review

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

Page 109: GI Review

WHAT IS THE GOLD STANDARD FOR DX OF

HIRSCHSPRUNG DISEASE

Rectal Biopsy

Page 110: GI Review

WHAT IS THE DEFINITION OF DIARRHEA?

Stool output >200gm/day

Increased frequency

Decreased consistency

Page 111: GI Review

PAIN, CRAMPING, DISTENSION, INABILITY TO

PASS GAS, HIGH PITCHED BOWEL SOUNDS

Intestinal Obstruction

Page 112: GI Review

WHAT IS AN IMPORTANT CAUSE OF

INTUSSUSCEPTION?

Neoplasm

Kids: enlarged lymph nodes

Page 113: GI Review

IN A POSTOP PATIENT WITH PSEUDO-

OBSTRUCTION, WHAT DRUG CAN BE USED IF

CONSERVATIVE RX FAILS?

Neostigmine

Page 114: GI Review

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

Page 115: GI Review

HOW SHOULD A DIAGNOSIS OF IBS BE MADE?

HPI

Rome criteria

DO NOT OVERTEST

Page 116: GI Review

SIGNS OF MALABSORPTION

Weight loss

Osteomalacia

Increased prothrombin time

Peripheral edema

Steatorrhea

Low albumin

Page 117: GI Review

WHAT IS THE DIAGNOSTIC TEST FOR LACTOSE

INTOLERANCE

Hydrogen Breath Test

Page 118: GI Review

WHAT CAN YOU TEST FOR CELIAC’S IN A

PATIENT WHO HAS BEEN ON A GLUTEN FREE

DIET?

HLA-DQ2/8

Page 119: GI Review

WHAT MALIGNANCY IS ASSOCIATED WITH

CELIAC’S DISEASE

T cell Lymphoma

Page 120: GI Review

WHAT ARE THE FOUR CARDINAL SYMPTOMS OF

WHIPPLE DISEASE

Arthralgia

Weight Loss

Diarrhea

Abdominal Pain

Also cardiac, pulmonary and CNS effects

CNS ISSUES!

Page 121: GI Review

WHAT ANTIBIOTIC SHOULD YOU GIVE FOR

WHIPPLE DISEASE?

Initial IV antibiotic that can cross BBB: Ceftriaxone

12 mo oral maintenance on Bactrim

Page 122: GI Review

WHAT TWO KEY LAB RESULTS CAN YOU SEE

WITH SIBO?

B12 Deficiency

Increased Folate due to synthesis from bacteria

Page 123: GI Review

HOW CAN YOU DIAGNOSE SIBO?

Jejunal Aspirate is gold standard, but a D-xylose breath test can be indicative

Page 124: GI Review

NAME THREE CONDITIONS WHERE THE PATIENT

SHOULD BE NPO

Diverticulitis

Acute Pancreatitis

Cholecystitis

Page 125: GI Review

NAME TWO ABX THAT CAN BE USED FOR SIBO.

Doxycycline, Rifaximin, Amoxicillin-clavulanate

Page 126: GI Review

WHICH PART OF THE GI TRACT DO VIRUSES

PRIMARILY ATTACK

Small Intestine

Page 127: GI Review

GIARDIA IS MOST OFTEN SEEN ON A BIOPSY OF

WHAT?

Duodenal Biopsy

Seen in spaces between duodenal villi

Page 128: GI Review

WHAT DO E. HISTOLYTICA TROPHOZOITES

INGEST THAT CAN BE SEEN ON BIOPSY TO

DISTINGUISH FROM MACROPHAGES

Red Blood Cells

Page 129: GI Review

THIS POLYMORPHISM IS ASSOCIATED WITH

CROHN’S DISEASE

NOD2

Page 130: GI Review

WHAT INDUCTION DRUG IS USED FOR UC BUT

NOT FOR CROHN’S

Sulfasalazine

Page 131: GI Review

CROHN’S DISEASE IS ASSOCIATED WITH THESE

TYPES OF T CELLS

TH1 and TH17

UC is TH1 and TH2

Page 132: GI Review

WHAT IS THE BEST METHOD OF

ADMINISTRATION FOR SULFASALAZINE?

Enema

Page 133: GI Review

NAME 3 IMPORTANT SIDE EFFECTS OF

GLUCOCORITCOIDS

Suppressed immune response

Cataracts

Osteoporosis

Page 134: GI Review

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

Page 135: GI Review

SKIP LESIONS, COBBLESTONE MUCOSA,

CREEPING FAT

Crohn’s

Page 136: GI Review

WHICH DRUG MUST NOT BE ADMINISTERED

WITH AZATHIOPRINE OR 6-MP

Allopurinol

Page 137: GI Review

WHAT IS THE MOST IMPORTANT ADVERSE

EFFECT OF TACROLIMUS AND CYCLOSPORINE

Renal Dysfunction

Page 138: GI Review

SERIOUS RISK OF PML

Natalizumab

Page 139: GI Review

NAME THE 3 HALLMARK SIGNS OF CHRONIC

MUCOSAL INJURY

Paneth Cell Metaplasia

Basal Plasmacytosis

Distortion of architecture

Crypt forking

Page 140: GI Review

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

Page 141: GI Review

WHAT KIND OF MONOCLONAL ANTIBODY IS

INFLIXIMAB?

Chimeric

Part mouse-part human

Page 142: GI Review

WHAT TEST MUST BE ADMINISTERED PRIOR TO

STARTING A PATIENT ON A TNF INHIBITOR

PPD TB test

Page 143: GI Review

DOES UC OR CROHN’S HAVE A HIGHER RISK OF

SUBSEQUENT NEOPLASIA?

UC

Page 144: GI Review

WHAT IS AN IMPORTANT CARDIAC SYMPTOM

OF CARCINOID SYNDROME?

Cardiac Valvular Fibrosis caused by Serotonin

Page 145: GI Review

WILL THE FECAL OSMOLAR GAP BE ELEVATED

IN CHOLERA?

No this is a secretory diarrhea

Page 146: GI Review

WHAT IS THE MAIN ANTIBIOTIC GIVEN FOR

CHOLERA?

Doxycyclin

Or azithromycin

Page 147: GI Review

ABUSE OF WHAT DRUGS CAN LEAD TO

OSMOTIC DIARRHEA?

Laxatives

Page 148: GI Review

MIDDLE AGED FEMALE WITH CHRONIC WATERY

DIARRHEA TAKING SERTRALINE

Collagenous Colitis

Rx: stop medications, loperamide, budesonide

Page 149: GI Review

DIFFERENTIAL FOR SECRETORY DIARRHEA

Cholera

ETEC

Collagenous Colitis

Lymphocytic colitis

Bile salt diarrhea

Neuroendocrine tumor

Laxative abuse

Page 150: GI Review

INFLAMMATORY DIARRHEA DIFFERENTIAL

Salmonella, Shigella, Campylobacter, C diff, Yersinia, Radiation, IBD, E.

Histolytica

Page 151: GI Review

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.

Page 152: GI Review

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.

Page 153: GI Review

ELEVATED BUN, NORMAL CREATININE, THINK…

Upper GI bleed

Page 154: GI Review

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.

Page 155: GI Review

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.

Page 156: GI Review

DIAGNOSTIC TEST FOR INFLAMMATORY

DIARRHEA?

Fecal Leukocytes/Lactoferrin

Page 157: GI Review

WHAT IS THE BEST TREATMENT FOR C.

DIFFICILE INFECTION?

Oral Metronidazole or Oral Vancomycin

Page 158: GI Review

PSEUDOMONAS COVERAGE

Page 159: GI Review

IN A PATIENT WITH SUSPECTED DIVERTICULITIS

WHAT DIAGNOSTIC TEST SHOULD YOU NOT DO?

Colonoscopy – POTENTIAL FOR PERFORATION

Page 160: GI Review

GERMLINE MUTATION OF LKB1/STK11 LEADS

TO THIS KIND OF INTESTINAL POLYP

Peutz-Jegher

Christmas tree appearance

Adenocarcinomas arise independently

Page 161: GI Review

WHAT IS THE MOST COMMON CANCER

ASSOCIATED WITH PEUTZ JEGHER?

Breast>colon>pancreas

Page 162: GI Review

JUVENILE POLYPS ARE ASSOCIATED WITH THIS

MUTATION…

SMAD4

Page 163: GI Review

WHAT IS THE MOST COMMON LOCATION FOR A

JUVENILE POLYP?

Rectum

Page 164: GI Review

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.

Page 165: GI Review

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

Page 166: GI Review

COLORECTAL CANCER T STAGE CHANGES FROM

1 TO 2 WITH INFILTRATION OF THIS LAYER.

Muscularis

Page 167: GI Review

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)

Page 168: GI Review

WHAT COLORECTAL CANCER HAS AN

INCREASED RISKED OF ENDOMETRIAL

CANCER?

HNPCC

Page 169: GI Review

WHAT IS THE MOST COMMON LOCATION OF

HNPCC?

Right sided

Page 170: GI Review

WHAT ARE THE TWO MAIN MANIFESTATIONS OF

PEUTZ JEGHER?

Mucocutaneous macules

Hamartomatous GI polyps

Muscular stalk

Malignancies arise de novo

Page 171: GI Review

WHY IS CARCINOID SYNDROME STRONGLY

ASSOCIATED WITH METASTASIS?

Vasoactive substances are metabolized to inactive forms in the liver

First pass

Page 172: GI Review

IN WHICH LOCATION OF THE GI TRACT ARE

CARCINOID TUMORS MOST AGGRESSIVE?

Small intestine

Page 173: GI Review

WHAT IS THE TYPICAL APPEARANCE OF A

CARCINOID TUMOR?

Trabecular architecture

Salt and pepper chromatin

Page 174: GI Review

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

Page 175: GI Review
Page 176: GI Review

WHAT IS THE DOC FOR LISTERIA?

Ampicillin

Page 177: GI Review

WHICH ANTIBIOTICS ARE BACTERIOCIDAL

Fluoroquinolones

TMP-SMX – Bactrim

Aminoglycosides

Page 178: GI Review

WHICH BACTERIA CAUSES MESENTERIC

LYMPHADENITIS (MIMICS APPENDICITIS)

Yersinia

Page 179: GI Review

WHAT IS THE TRIAD OF HUS

Renal Failure

Thrombocytopenia

Hemolytic anemia

Page 180: GI Review

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

Page 181: GI Review

WHICH BACTERIA CAN LEAD TO GUILLAIN

BARRE SYNDROME?

Campylobacter jejuni

Page 182: GI Review

WHAT AGE IS MOST COMMON FOR INFECTION

BY H. PYLORI

<5 years

Page 183: GI Review

WHICH BACTERIA ONLY HAS A HUMAN HOST?

Shigella

Page 184: GI Review

WHAT IS THE BEST TREATMENT FOR SHIGELLA?

Azithromycin or Bactrim

Campylobacter can also be treated with azithromycin

Page 185: GI Review

WHAT FORM OF GIARDIA IS TRANSMITTED AND

WHAT FORM CAUSES DISEASE?

Cysts are transmitted

Trophozoites cause disease

Page 186: GI Review

WHAT IS THE TEST OF CHOICE FOR GIARDIA

Antigen

Page 187: GI Review

WHAT IS THE TREATMENT OF CHOICE FOR

CRYPTOSPORIDIUM

Immunocompetent: Nitazoxanide

AIDS: HAART

Page 188: GI Review

WHAT ARE THE TWO MAJOR REASONS FOR

FAILURE OF H. PYLORI TREATMENT?

Poor patient compliance

Antibiotic resistance

Clarithromycin, amoxicillin, omeprazole

Metronidazole, tetracycline, bismuth, omeprazole

Page 189: GI Review

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

Page 190: GI Review

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)

Page 191: GI Review

THIS PARASITIC INFECTION HAS A HIGH RISK

OF CHOLANGIOCARCINOMA DUE TO

HYPERPLASIA AND FIBROSIS OF THE BILIARY

TRACT

Clonorchis – Liver Fluke

Treat with Praziquantel

Page 192: GI Review

DESCRIBE WHAT SUBSTANCES NOROVIRUS

CAN RESIST?

Resistant to chlorine AND alcohol

Must use 1:10 bleach – VERY TRICKY ON CRUISE SHIPS

Page 193: GI Review

WHY DOES NOROVIRUS USUALLY ONLY LAST 24

HOURS?

Can only infect mature enterocytes and epithelial turn over eliminates mature

enterocytes in that time period.

Page 194: GI Review

WHAT IS A SEAGULL SHAPED BACTERIA

Campylobacter Jejuni

Page 195: GI Review

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.

Page 196: GI Review

WHICH ORGANISM AND SPECIFIC TOXIN ARE

ASSOCIATED WITH FRIED RICE?

Bacillus Cereus

Heat Stable toxin

Page 197: GI Review

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

Page 198: GI Review

WHAT IS THE DOC FOR C. DIFFICILE

Oral metronidazole

Oral vancomycin

Page 199: GI Review
Page 200: GI Review

WHAT IS THE NAME OF THE THIN LAYER OF

CONNECTIVE TISSUE THAT COVERS THE LIVER?

Glisson’s capsule

Page 201: GI Review

TWO IMPORTANT ENZYMES IN THE LIVER FOR

DRUG METABOLISM ARE…

Cytochrome p450

Glucouronyl Transerase

Page 202: GI Review

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.

Page 203: GI Review

WHICH CELLS IN THE LIVER ARE CRUCIAL FOR

REGENERATION IN FIBROSIS AND CIRRHOSIS?

Ito (Stellate) cells

Page 204: GI Review

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.

Page 205: GI Review

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

Page 206: GI Review

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

Page 207: GI Review

ACUTE HEPATITIS HISTOLOGY?

Lobular lymphocytes

Balooning degeneration

Page 208: GI Review

CHRONIC HEPATITIS HISTOLOGY?

Periportal lymphocytes Zone 1

Piecemeal necrosis

Acidophil bodies

Fibrosis

Page 209: GI Review

ALD AND NAFLD HISTOLOGY?

Steatosis – Zone 3

Neutrophilic infiltrate

Mallory hyaline bodies

Sclerosing hyaline necrosis – fibrosis around central vein

Page 210: GI Review

SOLITARY WELL CIRCUMSCRIBED LIVER MASS

WITH HIGH RISK POTENTIAL FOR

INTRATUMORAL HEMORRHAGE

Hepatic adenoma

Caused by birth control or steroids

Page 211: GI Review

MOST COMMON BENIGN TUMOR OF THE LIVER?

Hemangioma

Page 212: GI Review

WHAT MARKER IS OFTEN ELEVATED IN

HEPATOCELLULAR CARCINOMA

Alpha Fetoprotein

VERY POOR PROGNOSIS

Page 213: GI Review

ALT IS FOUND IN THE WHILE AST IS

FOUND IN THE

Liver cytosol

Liver, skeletal and cardiac muscle, brain and kidney

Page 214: GI Review

5’ NUCLEOTIDASE IS A MARKER OF…

Disease of Hepatobiliary origin

Page 215: GI Review

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

Page 216: GI Review

BILIRUBINURIA IS EVIDENCE OF…

Direct/Conjugated Hyperbilirubinemia

Page 217: GI Review

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

Page 218: GI Review

TREATMENT FOR AUTOIMMUNE HEPATITIS IS?

Prednisone

Can taper to Azathioprine

Page 219: GI Review

ASIAN POPULATIONS MAY LACK THIS ENZYME

CAUSING BUILD UP OF TOXINS LEADING TO

FLUSHING AND TACHYCARDIA

ALDH

Page 220: GI Review

WHAT ARE THE SYMPTOMS OF HEREDITARY

HEMOCHROMATOSIS?

Bronze Diabetes

Fatigue

Exocrine and endocrine pancreatic dysfunction

Hepatomegaly

Cardiac conduction dysfunction

Joint arthralgais

Page 221: GI Review

WHAT ARE THE TWO PRIMARY MUTATIONS OF

HH?

C82Y

H63D

Of the HFE gene on chromosome 6

Transferrin sat >50% is pathognomonic

Page 222: GI Review

LIVER DISEASE WITH CONCOMITANT

NEUROPSYCHIATRIC DISEASE IN ADOLESCENTS

Wilson’s

Kaiser-Fleischer rings

Basal ganglia are affected

Page 223: GI Review

LAB RESULTS FOR WILSON’S DISEASE

Low ceruloplasmin

High urinary copper

Page 224: GI Review

XANTHEMATOUS LESIONS, ELEVATED ALK

PHOS, FLORID DUCT LESIONS, AMA, ANA,

GRANULOMAS

Primary Biliary Cirrhosis

Autoimmune destruction of small intrahepatic ducts

Page 225: GI Review

WHAT IS THE TREATMENT FOR PBC?

Urdeoxycholic Acid

Page 226: GI Review

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!

Page 227: GI Review

PAINFUL HEPATIC ENLARGEMENT, JAUNDICE,

SPLENOMEGALY WITH HYPERCOAGULABILITY

OR A PROMINENT CAUDATE LOBE

Budd Chiari

Dx with Doppler Ultrasound

Page 228: GI Review

3 EXAMPLES OF AGENTS CAUSING DIRECT

DRUG INDUCED LIVER DISEASE

Acetaminophen (depletes glutathione)

Alcohol

Statins

Tetracyclins

Niacin

Valproic acid

Page 229: GI Review

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

Page 230: GI Review

WHAT ARE THE SYMPTOMS OF PORTAL

HYPERTENSION?

Jaundice

Scleral icterus

Palmar erythema

Spider angiomata

Gynecomastia

Testicular atrophy

Caput medusae

Ascites

Low platelets

asterixis

Page 231: GI Review

IF SAAG IS >1.1 SUSPECT…

Portal Hypertension

If protein >2.5 suspect CHF or Budd Chiari

Page 232: GI Review

WHAT IS THE TREATMENT FOR ASCITES?

Salt restriction

Spirolactone – potassium sparing

Furosemide

Therapeutic large volume paracentesis

Consider TIPS - but not before getting an ECHO!!

Page 233: GI Review

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

Page 234: GI Review

WHAT IS THE BEST TREATMENT FOR SBP?

Cephalosporin

Prophylactic Cipro or Bactrim

E. Coli is most common (gram + cocci also)

ALSO AMP-SULF

Page 235: GI Review

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

Page 236: GI Review

WHAT IS THE TREATMENT FOR HEPATIC

ENCEPHALOPATHY?

Lactulose – acidifies the colon

Rifaximin – eliminates ammonia producing bacteria

DO NOT MONITOR AMMONIA AS A MARKER

Page 237: GI Review

NAME TWO PHYSICAL EXAM FINDINGS FOR

HEPATOPULMONARY SYNDROME

Platypnea – greater dyspnea in seated position than recumbent

Orthodeoxia – arterial deoxygenation in seated position

Page 238: GI Review

WHAT ARE THE THREE MEASURES OF MELD

INR

Creatinine

Total Bilirubin

Page 239: GI Review

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

Page 240: GI Review

WHAT DIAGNOSTIC TEST IS CONTRAINDICATED

WITH AN AMEBIC ABSCESS?

Biopsy can cause peritoneal spilling and peritonitis

Page 241: GI Review

NAME THE BENIGN LIVER LESIONS

Hemangioma

Hepatic adenoma

Focal nodular hyperplasia

Page 242: GI Review

WHAT IS THE CHARACTERISTIC FINDING OF A

HEMANGIOMA ON IMAGING?

Peripheral enhancement with delayed central filling

Page 243: GI Review

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

Page 244: GI Review

NAME THE TWO MOST COMMON MODALITIES

OF TREATMENT FOR HCC

Trans-arterial Chemoembolization

Radiofrequency Ablation

Page 245: GI Review

WHAT ARE THE MILAN CRITERIA FOR LIVER

TRANSPLANTATION?

3 HCC lesions less than 3 cm or 1 lesion less than 5cm

Page 246: GI Review

WHAT ARE THE FOUR F’S OF CHOLESTEROL

CHOLELITHIASIS?

Female

Fat

Fertile

Forty

Page 247: GI Review

WHAT ARE THE INDICATIONS FOR A

CHOLECYSTECTOMY?

Pain

Calcified gallbladder (porcelain)

Stone > 3cm

Polyp > 1 cm

Page 248: GI Review

WHAT PROPHYLACTIC MEASURES CAN BE

TAKEN IN A BARIATRIC SURGERY TO REDUCE

FORMATION OF GALLSTONES

Prophylactic cholecystectomy

Ursodeoxycholic acid

Page 249: GI Review

WHAT RISKS DOES PORCELAIN GALLBLADDER

HAVE?

50% chance of malignancy

REMOVE!

Page 250: GI Review

SEVERE RUQ PAIN, VOMITING, FEVER, +

MURPHY’S SIGN, HIGH WBC (NO JAUNDICE)

Acute Cholecystitis

Page 251: GI Review

WHAT IS THE MOST SENSITIVE TEST FOR ACUTE

CHOLECYSTITIS/CYSTIC DUCT BLOCKAGE?

HIDA scan

Page 252: GI Review

WHAT IS REYNOLD’S PENTAD?

Indications of ascending cholangitis

Fever

Jaundice

RUQ pain

Altered mental status

Hypotension

Page 253: GI Review

WHAT IS THE TREATMENT FOR CHOLANGITIS?

ERCP and Pip-tazo/amp-sulf/mero (life threatening)

Also cip + metro

Page 254: GI Review

NAME TWO CONDITIONS THAT INCREASE RISK

FOR CHOLANGIOCARCINOMA

PSC

Choledochal cyst

Diverticulae

Parasitic infections from Asia

Klatskin tumor

Gray nodular infiltrative growth

Page 255: GI Review

HOW IS DIAGNOSIS OF A GALLSTONE ILEUS

MADE?

CT or XRAY demonstrating pneumobilia

Surgical removal needed

Page 256: GI Review

BORING EPIGASTRIC PAIN RADIATING TO BACK

WITH NAUSEA VOMITING ANOREXIA AND

WORSENING PAIN WITH WALKING OR LYING

Acute Pancreatitis

Elevated lipase

Page 257: GI Review

WHAT TWO SIGNS ARE WORRISOME FOR

NECROTIZING PANCREATITIS

Cullen’s sign – bruising around umbilicus

Turner’s sign – flank bruising

Page 258: GI Review

WHAT ARE THE TWO MOST COMMON

ETIOLOGIES OF ACUTE PANCREATITIS

Alcohol

Gallstones

Page 259: GI Review

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

Page 260: GI Review

WHAT ARE THE MOST DESMOPLASTIC

TUMORS?

Pancreatic ductal adenocarcinoma

Page 261: GI Review

WHAT IS THE STANDARD TREATMENT FOR

ACUTE PANCREATITIS?

NPO

Fluid resuscitation

Pain management

Potential for TPN

Page 262: GI Review

NAME THREE COMPLICATIONS OF ACUTE

PANCREATITIS

Pancreatic Ascites

Third spacing – Volume depletion

Acute kidney failure

Shock

ARDS (respiratory failure)

Necrosis/infection/abscess

Pseudcocyst

Page 263: GI Review

WHAT IS THE BEST TREATMENT FOR

AUTOIMMUNE PANCREATITIS?

Steroids

Page 264: GI Review

WHAT COMPLICATIONS ARE ASSOCIATED WITH

CHRONIC PANCREATITIS

Duodenal Obstruction

Biliary stricture

Pseudocyst

Cancer

Page 265: GI Review

HIGH ALK PHOS OR BILI WITHOUT EVIDENCE OF

BILIARY DISEASE….

Infiltrative or metastatic disease!

Page 266: GI Review

EPIGASTRIC PAIN, STEATORRHEA, DIABETES

Chronic pancreatitis

ALCOHOL, divisum

Fibrosis and calcification (visible on CT often)

ERCP is best for diagnosis

Page 267: GI Review

WHAT IS THE NUMBER ONE CAUSE OF

NEONATAL JAUNDICE?

Biliary atresia

Also the main cause of liver transplants in children

Page 268: GI Review

WHAT SHOULD YOU THINK OF WITH A VERY

LOW ALKALINE PHOSPHATASE?

Acute Wilson’s Disease

Page 269: GI Review

WHAT IS THE CAUSE OF STRAWBERRY

GALLBLADDER?

Cholesterolosis – cholesterol builds up in macrophages within lamina propria

Page 270: GI Review

WHAT IS A CRITICAL STEP IN A

CHOLECYSTECTOMY?

Demonstrate there are no stones in the common bile duct

Page 271: GI Review
Page 272: GI Review

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

Page 273: GI Review

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.

Page 274: GI Review

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)

Page 275: GI Review

DO CF PATIENTS EXPERIENCE OSMOTIC

DIARRHEA OR SECRETORY DIARRHEA?

Secretory Diarrhea – bacteria hydrolyze fats hydroxy fatty acids stimulate

cAMP which leads to secretory diarrhea

Page 276: GI Review

WHAT IS THE BEST MANAGEMENT PANCREATIC

INSUFFICIENCY DUE TO CYSTIC FIBROSIS?

Pancreatic enzymes

PPIs

High fat diet

Vitamin supplements

Page 277: GI Review

DESCRIBE THE CLINICAL PRESENTATION OF

PYLORIC STENOSIS

Nonbilious projectile vomiting usually between 1-5 weeks of age

Regurgitation

Dehydration

Infant hungry after vomiting

Page 278: GI Review

COMPARE THE PREVALENCE OF PYLORIC

STENOSIS BETWEEN MALES AND FEMALES

F – 1/1000

M – 5/1000

Page 279: GI Review

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

Page 280: GI Review

DESCRIBE THE MODE OF INHERITANCE OF

HEREDITARY HEMOCHROMATOSIS

Autosomal recessive

Page 281: GI Review

WHAT ARE THE RISKS OF 1ST, 2ND, AND 3RD

DEGREE RELATIVES OF CARRIERS?

1st: 1/2

2nd: 1/4

3rd: 1/8

Page 282: GI Review

WHAT IS THE BEST TEST FOR DIAGNOSIS OF

HEREDITARY HEMOCHROMATOSIS

Serum transferrin saturation

RX: Phlebotomy 1-2x/week until 25-50mg ferritin/L

Page 283: GI Review

PHLEBOTOMY CAN ALLEVIATE MOST OF THE

SYMPTOMS OF HEREDITARY HEMOCHROMATOSIS

EXCEPT…

Arthritis

Page 284: GI Review

NAME THREE COPPER RICH FOODS THAT

SHOULD BE AVOIDED IN WILSON’S DISEASE

Nuts

Chocolate

Mushrooms

Shellfish

Page 285: GI Review

IN WILSON’S DISEASE DO HEPATIC OR

NEUROLOGIC SYMPTOMS TYPICALLY PRESENT

FIRST?

Hepatic

Page 286: GI Review

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

Page 287: GI Review

WHAT IS THE BEST TREATMENT FOR CHRONIC

RETENTIVE CONSTIPATION IN PEDIATRIC PTS.?

Oral disimpaction

24 hr liquid diet

Golytely

Behavioral Modification

Page 288: GI Review

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.

Page 289: GI Review

FOOD IMPACTION WITH HISTORY OF ASTHMA,

ATOPIC DERMATITIS OR ALLERGIC RHINITIS

Eosinophilic Esophagitis

Page 290: GI Review

WHAT CONSERVATIVE MEASURE OFTEN

ALLEVIATES SYMPTOMS OF EOE

Elimination of allergic foods

Page 291: GI Review

WHAT IS A KEY GROSS FINDING OF

LATE/SEVERE EOE?

Trachealization of the esophagus

Strictures

Page 292: GI Review
Page 293: GI Review

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

Page 294: GI Review

NAME TWO RADIOLOGICAL FINDINGS FOR

ACUTE PANCREATITIS

Diffuse enlargement with peripancreatic inflammation (fat stranding)

Fluid collection – abscess or pseudocyst

Page 295: GI Review

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

Page 296: GI Review

WHAT ARE THE NORMAL DIAMETERS OF THE

SMALL INTESTINE, TRANSVERSE COLON AND

CECUM

3, 6, 9

Page 297: GI Review

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

Page 298: GI Review

WHAT IS THE BEST IMAGING FOR ACUTE

CHOLECYSTITIS?

Ultrasound

Page 299: GI Review

WHAT IS THE BEST IMAGING FOR

DIVERTICULITIS?

CT

Page 300: GI Review

WHAT ARE THE RADIOLOGICAL FINDINGS OF A

PERFORATED VISCUS?

Free air on AXR

Page 301: GI Review

WHAT ARE THE RADIOLOGICAL FINDINGS FOR

SMALL BOWEL OBSTRUCTION?

Dilated small bowel loops

Ladder like air fluid levels

Page 302: GI Review

RADIOLOGICAL FINDINGS FOR CECAL AND

SIGMOID VOLVULUS

Coffee bean

Sigmoid : LLQ

Cecal : RLQ

Page 303: GI Review

WHAT RADIOLOGICAL SIGN IN THE ILEUM CAN

INDICATE CROHN’S DISEASE?

String sign

Nodularity and ulceration

Page 304: GI Review

WHAT SHOULD YOU LOOK FOR ON A CT FOR

SUSPECTED APPENDICITIS?

Distended appendix with hyperenhancement and periappendiceal fat stranding

Page 305: GI Review

WHAT IS THE CLASSIC RADIOLOGICAL SIGN OF

COLON CANCER?

Apple core lesion

Page 306: GI Review
Page 307: GI Review

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

Page 308: GI Review

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.

Page 309: GI Review

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.

Page 310: GI Review

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

Page 311: GI Review

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

Page 312: GI Review

“FEAR OF EATING” – CHRONIC POST PRANDIAL

PAIN AND WEIGHT LOSS

Intestinal angina

Manage atherosclerosis

Stenting

Mesenteric bypass

Page 313: GI Review

DIAGNOSIS AND TREATMENT OF

AORTOENTERIC FISTULA?

Endoscopy

Emergent laparotomy

Most common in 3rd and 4th parts of the duodenum


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