USMLE STEP 1

GASTROINTESTINAL
TRACT
NOTES
Prepared By:
Dr. TA7
First Edition

Combination of:
First aid & U-WORLD extra facts
In an organized, concise & interesting blend

Dr. TA7
more and shine to help everyone.

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 GASTROINTESTINAL

Contents:

03 Embryology

08 Anatomy & Histology

10 Physiology

22 Pathology

9 Pharmacology
In Pharmacology TA7 Book

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 CHAPTER 1: GASTROINTESTINAL TRACT EMBRYOLOGY
Gut tube
- Foregut—esophagus to duodenum at level of pancreatic duct and common bile duct insertion (ampulla of
Vater).
- Midgut—lower duodenum to proximal 2/3 of transverse colon.
- Hindgut—distal 1/3 of transverse colon to anal canal above pectinate line.
- Midgut is characterized by the following:
* 6th week of development—physiologic herniation through umbilical ring
* 10th week of development—returns to abdominal cavity + rotates around superior mesenteric artery (SMA),
total 270° counterclockwise to place each component in its proper place in the abdominal cavity

Ventral abdominal wall defects

- Def— Developmental defects due to failure of rostral fold closure (e.g., sternal defects [ectopia cordis]), lateral
fold closure (e.g., omphalocele, gastroschisis), or caudal fold closure (e.g., bladder exstrophy).

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- Ectopia cordis— a very rare congenital condition in which the heart ends up outside of the thoracic cavity. This
occurs when lateral folds fail to fuse to form the thoracic wall during the fourth week, resulting in abnormal
development of the sternum and pericardium. Most affected infants die shortly after birth due to cardiac failure,
hypoxemia, or infection, but surgery can be attempted as long as there are no severe cardiac defects.

Congenital umbilical hernia

- Cause— Failure of umbilical ring to close after physiologic herniation of midgut.
- Characters
* Covered by skin
* Protrudes with increase intra-abdominal pressure (e.g., crying)
- Associations— Other congenital anomalies e.g., Down syndrome, congenital hypothyroidism
- Treatment— Small defects usually close spontaneously otherwise, surgery is recommended

Tracheoesophageal anomalies
- Esophageal atresia (EA) with distal tracheoesophageal fstula (TEF):
* Most common type (85%)
* Presents as polyhydramnios in utero (due to inability of fetus to swallow amniotic fluid). Neonates drool,
choke, and vomit with first feeding.
* TEFs allow air to enter stomach (visible on CXR as prominent gastric air bubble)
* Complication  Cyanosis 2° to laryngospasm (to avoid reflux-related aspiration)
* Diagnosis  failure to pass nasogastric tube into stomach
- Other types:
* Pure EA or stenosis  Gasless abdomen
* Pure TEF (H type)  the fistula resembles the letter H

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 Intestinal atresia

- Jejunal and ileal atresia—disruption of mesenteric vessels (typically SMA)  ischemic necrosis of fetal intestine
 segmental resorption: bowel becomes discontinuous (apple peel). X-ray may show “triple bubble” (dilated
stomach, duodenum, proximal jejunum) and gasless colon. Associated with cystic fibrosis. May be caused by
maternal cigarette smoking or use of vasoconstrictive drugs (e.g., cocaine) during pregnancy.

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 Hypertrophic pyloric stenosis
- Most common cause of gastric outlet obstruction in infants (usually in 1st born male)
- Manifestations— Palpable olive-shaped mass in epigastric region, visible peristaltic waves, and nonbilious
projectile vomiting at ∼ 2–6 weeks old
- Complications— hypokalemic hypochloremic metabolic alkalosis (2° to vomiting of gastric acid and subsequent
volume contraction)
- Diagnosis— Ultrasound shows thickened and lengthened pylorus
- Treatment— surgical incision of pyloric muscles (pyloromyotomy)

Intestinal malrotation
- Incidence— symptomatic malrotation (midgut volvulus) in 1:6000 live births in the United States
- Pathophysiology— arrest in the normal rotation of the gut in utero, resulting in an abnormal orientation of the
bowel and mesentery within the abdominal cavity
- Types
* Nonrotation  The entire colon is left-sided; the entire small bowel is right-sided
* Incomplete rotation  The cecum remains fixed in the RUQ by peritoneal bands (Ladd bands)
* Midgut volvulus  torsion of a malrotated midgut causing mechanical bowel obstruction
- Manifestations— Malrotation: mostly asymptomatic, Midgut volvulus (Bilious emesis + Intestinal obstruction)
- Management— Surgery

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 Hypertrophic pyloric stenosis
- Most common cause of gastric outlet obstruction in infants (usually in 1st born male)
- Manifestations— Palpable olive-shaped mass in epigastric region, visible peristaltic waves, and nonbilious
projectile vomiting at ∼ 2–6 weeks old
- Complications— hypokalemic hypochloremic metabolic alkalosis (2° to vomiting of gastric acid and subsequent
volume contraction)
- Diagnosis— Ultrasound shows thickened and lengthened pylorus
- Treatment— surgical incision of pyloric muscles (pyloromyotomy)

Intestinal malrotation
- Incidence— symptomatic malrotation (midgut volvulus) in 1:6000 live births in the United States
- Pathophysiology— arrest in the normal rotation of the gut in utero, resulting in an abnormal orientation of the
bowel and mesentery within the abdominal cavity
- Types
* Nonrotation  The entire colon is left-sided; the entire small bowel is right-sided
* Incomplete rotation  The cecum remains fixed in the RUQ by peritoneal bands (Ladd bands)
* Midgut volvulus  torsion of a malrotated midgut causing mechanical bowel obstruction
- Manifestations— Malrotation: mostly asymptomatic, Midgut volvulus (Bilious emesis + Intestinal obstruction)
- Management— Surgery

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 CHAPTER 2: GASTROINTESTINAL TRACT MICRO-ANATOMY

PLEASE NOTE THAT DETAILED GIT GROSS ANATOMY WILL BE DISCUSSED IN GENERAL ANATOMY

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 Intestinal alkalinity
- Importance— neutralization of the gastric contents to protect the intestinal mucosa from damage
- Sources
1- Brunner glands
= Secrete large amounts of alkaline mucus into the duodenum (crypts of Liberkeihn).
= Most numerous at the pylorus but, may be found up to the ampulla of Vater.
2- Pancreatic secretion = epithelial cells of the pancreatic ductules and ducts produce watery secretions
containing high concentrations of bicarbonate ions
- Induced by
1-Tactile stimulation of the duodenal mucosa.
2-↑parasympathetic activity following meals.
3-The presence of acid in the duodenum and jejunum

Peyer’s patches
- Contains specialized cells called M cells + lymphoid aggregates
- M cells act as an antigen presenting cells which engulf any GIT antigen and degrade it into fragments which are
presented to the T helper cells to initiate an acquired immune response against the antigen
- M cells are specifically designed to sample the contents of the gut lumen and transfer antigens to their basal
lamina within endosomes

Paneth cells
- Site— Small group of cells at the base of intestinal crypts
- Functions— phagocytic and secretory properties = first line of immune defense against intestinal
microorganisms
- Secretion— lysozyme, an enzyme which destroy the cell wall of bacteria, and defensins, antimicrobial and
antiparasitic polypeptides

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CHAPTER 3: GASTROINTESTINAL TRACT PHYSIOLOGY

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 Secretin stimulation test: Administration of exogenous secretin stimulates gastrin release from gastrinomas

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 Postprandial alkaline tide: increase in plasma HC03 and decrease in plasma Chloride secondary to the surge of
acid within the gastric lumen.
 Gastric venous blood alkalosis: Gastric venous blood has a higher PH than arterial due to increased HCO3-
reabsorption into veins during synthesis of HCL

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CHAPTER 4: GASTROINTESTINAL TRACT PATHOLOGY

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 Zenker diverticulum can lead also to pulmonary aspiration symptoms like cough, dyspnea and stridor
due to regurgitation

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• Meckel’s diverticulum can have ectopic mucosa (usually gastric mucosa) which can secrete HCL causing
intestinal ulceration and maldigestion due to inactivation of intestinal enzymes. This is called ectopy or
heterotropy or Choristoma

• Visualization of Meckel diverticulum can be done by Technetium scan which show ectopic gastric mucosa
if present

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 Liver & pancreas pathology

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• HyperNH3 causes dysfuntion in aa transport across BBB leading to alteration in
neurotransmitte\r synthesis/metabolism ➔ + GABA, - Glutamate {CNS suppression}

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 * Aflatoxin acts by mutation of p53 tumor suppressor gene
causing uncontrolled cell cycle proliferation

*CD31 (PECAM) positive = marker of endothelial cells

* Hepatoblastoma: is the most common liver tumor in pediatrics. It is associated with familial polyposis syndrome
and beckwith widedman syndrome. It has characteristic microscopic picture including small rounded malignant cells
and mixed mesechymal tissues e.g., cartilage. It is usually fatal if not resected.

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* Don't rely only on Kayser Fleicher ring to diagnose wilson disease because it is associated also with any
disease causing cholestasis. You have to confirm diagnosis with genetic analysis.

* Both iron and lipofuscin looks brown by H&E staining = to differentiate stain with prussian blue

* (+) ALP and cholestrol

without jaundice may be
the presentation
* C/P: fever, pruritis, jaundice (may be), hypercholestrolemia

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 * Hepatocyte injury can cause
pigment gall stones due to
release of glucuronidase
enzyme leading to dissociation
of glucuronic acid from bilirubin
which become less soluble
* Another RF for gall stones is total parentral nutrition
due to decreased food induced intestinal hormonal
secretion causing (-) CCK leading to (-) gall bladder
and biliary tract motility (biliary stasis). This is called
biliary sludge with muddy bile ppt in the gall bladder
(due to over concentration of bile)

* Bile has lecithinase so, its

stasis leads to destruction of
lecithin in protective mucous
layer in gall bladder so, bile
salts can irritate gall bladder
wall + increased pressure =
inflammation & ischemia

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Pancreas pathology

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 ABOUT THE AUTHOR:
Mohammed Abdel-Fattah (Dr. Ta7) who is a USMLE lecturer in TA7
USMLE preparation system for about 15 years of experience in
USMLE step 1 education as a lecturer and he is USMLE step 1 and
step 2 CK certified. He made 2 clinical rotations
in USA:
- Psychiatry: Case western reserve university hospitals.
- Neurology: Institute of neuroscience (JFK medical center).

CONTACT US:

Dr. TA7 Facebook: https://www.facebook.com/dr.ta7.usmle

Dr. TA7 E-Mail: [email protected]

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