Exam I

Question 1

Physio: These cells are in the muscularis mucosa, and secrete pepsinogen, lipase and leptin.

Secretion is activated by HCl and Ach (inc. pepsinogen)

Answer 1

Chief cells

*pepsinogen – cleaved; protein metabolism

Question 2

Physio: These cells are located in the body of the stomach and secrete HCl and IF.

Secretion is stimulated by histamine, gastrin and Ach (PNS).

Answer 2

Parietal cells

Question 3

Physio: These cells are located in the antrum of the stomach. They secrete gastrin which stimulate parietal cells to secrete HCl

Answer 3

G-cells

Question 4

Physio: These cells secrete trefoil factors (protective coating for the stomach) and are located in the antrum

Answer 4

Mucous cells

Question 5

Physio: Histamine and Somatostatin are paracrines. Where do they originate and what are their functions?

Answer 5

1. Somatostatin
   - -D cells
   - -inhibit gastric acid secretion
   stimulus: pH < 3
2. Histamine
   - -increase gastric acid secretion

Question 6

Physio: CCK is a hormone that is secreted from I cells. It is stimulated by fats, peptides, and amino acids.

What are its functions?

a. Inc. gallbladder activity (bile secretion)
b. Increase pancreas activity (HCO3-)
c. Increase growth of the pancreas
d. Decrease gastric motility/secretions and emptying

Answer 6

All of the above

Question 7

Physio: A hormone secreted by S-cells. It is stimulated by fat and acid, and functions to increase HCO3- from the pancreas.

Answer 7

Secretin

• nature’s antacid
• dec. gastric acid

Question 8

Physio: A hormone that is stimulated by all 3 food groups (lipids, proteins, and glucose). It functions to increase insulin and decrease gastric acid

Answer 8

GIP

Question 9

Physio: A candidate hormone from the M-cells of the upper duodenum that stimulates the migrating (myoelectric) motor complex.

Answer 9

Motilin

• fasting state
• erythromycin stimulates

Question 10

Physio: Alpha cells of the pancreas produce

Answer 10

glucagon

Question 11

Physio: Beta cells of the pancreas produce

Answer 11

Insulin

Question 12

Physio: F-cells secrete _______, a candidate hormone which functions to ______

Answer 12

Pancreatic polypeptide

Fxn: Decrease pancreatic enzyme secretion; dec. HCO3-
Stimulus: Cho, protein, lipid ingestion

Question 13

Physio: Acid secretion occurs in 3 phases:

1. The cephalic phase: mediated by the ______ nerve. It is triggered by taste, sight, smell and thought of food.
2. The _____ phase: food enters the stomach, causing release of gastrin and stimulation of Histamine and Hcl
3. Intestinal phase: protein enters the duodenum. Overall effect reduces acid secretion. _____ is released which acts on enterochromaffin-like cells (inhibits histamine).

Answer 13

1. vagus
2. gastric
3. Peptide YY

Question 14

Physio: _____ factilitates HCO3- and mucous production

Answer 14

prostaglandin E

Question 15

Physio: The exocrine pancreas secretes electrolytes and inactive ensymes (zymogens) which are activated upon entering the duodenum.

Pancreatic secretions are normally ___ with plasma

Answer 15

Isotonic

• HCO3- neutralize
• Enzymes involved in digestion of fat, carbs protein

Question 16

Physio: Colipase is a cofactor that is secreted by the pancreas. What is its function?

Answer 16

Inc. efficiency of lipase

Question 17

Physio: Large dietary lipids are primarily digested in the duodenum by pancreatic enzymes such as

Answer 17

1. cholesterol esterase
2. lipase
3. phospholipase A2

Question 18

Physio: _______ aid in lipid metabolism by emulsifying the fatty acids and monoglycerides into micelles

Answer 18

bile salts

*fa’s can then diffuse into enterocytes where they are packaged into chylomicrons and delivered to lymph.

Question 19

Physio: Lipid absorption occurs primarily in the

Answer 19

jejunum

Question 20

Physio: The main function of pepsin is

Answer 20

proteolysis

*other proteases activated by trypsin

Question 21

Physio: Iron is absorbed in the duodenum as

Answer 21

Fe2+

*in alkaline env. = Fe3+

Question 22

Physio: A candidate hormone that arises from Intestinal cells in response to fat and hypOglycemia. It increases hepatic glycogenolysis and gluconeogenesis.

Answer 22

Enteroglucagon

*inc. glucose production in reponse to low glucose

Question 23

Physio: A candidate hormone that arises from intestinal L cells. It is secreted in response to HypERglycemia. It stimulates glucose-dependent insulin (B-cells) secretion, decreases glucagon and decreases gastric emptying

a. GLP-1
b. Pepsin
c. Enteroglucagon
d. Ghrelin

Answer 23

Glucagon-like peptide 1

I = inhibit

**Incretin

Question 24

Physio: Which of the following decreases anorexigenic neurons, increases orexigenic neurons and promotes appetite?

a. Ghrelin
b. Peptide YY
c. GLP-1
d. Insulin
e. Leptin

Answer 24

Ghrelin

**Hypothalamus:
Satiety center: ventromedial nucleus of hypothalamus
Feeding center: LHA (lateral nucleus of hypothalamus)

Question 25

Physio: Which of the following substances promotes appetite by inhibiting anorexigenic neurons, and stimulating orexigenic neurons?

a. Ghrelin
b. Peptide YY
c. GLP-1
d. Insulin
e. Leptin

Answer 25

Ghrelin

**Hypothalamus: VPN, LHA

Question 26

Physio: Which of the following Neurotransmitters is responsible for smooth muscle contraction and relaxation of sphincters?

a. acetylcholine
b. NE
c. VIP
d. GRP

Answer 26

Ach

• inc. salivary secretion
• inc. gastric secretion
• inc. pancreatic secretion

*PNS

Question 27

Physio: Norepinephrine, Neuropeptide Y and VIP all play a role in relaxing the smooth muscle of the GI tract.

1. _________ constricts sphincters and increases saliva.
2. _______ inc. intestinal and pancreatic secretion.
3. _______ decreases intestinal secretions.

Answer 27

1. NE
   - -contract spincters
   - -salivary secretion
2. VIP
   - -inc. intestinal and pancreatic secretion
3. Neuropeptide Y
   - -dec. intestinal secretions

Question 28

Physio: Substance P is secreted with Acetylcholine. What is its role?

Answer 28

SM contraction

*inc. salivary secretion

Question 29

Physio: Enkephalins are neutrotransmitters that play a role in _______ GI motility and decreasing intestinal secretions.

Answer 29

Decrease GI motility

Question 30

Physio: Leptin is a substance that is secreted by fat cells in response to body fat levels. What is the function of this substance?

Answer 30

Decrease appetite

inc. anorexigenic, dec. orexigenic

Question 31

Physio: The 3 phases of swallowing are:

1. _____ phase: Tongue forces bolus back to pharynx
2. _____ phase: The soft palate is pulled upward, the epiglottis covers the larynx, and the UES relaxes.
3. _____ phase: The UES closes, and the primary peristaltic wave propels food. Receptive relaxation occurs here.

Answer 31

1. ORal
2. Pharyngeal
   - -peristalsis propels bolus through UES
3. Esophageal
   - -UES closes
   - -primary and secondary peristatltic waves
   - -Receptive relaxation (LES opens)
   - -LES closes

Question 32

Physio: Gastric motility is inhibited by the SNS and stimulated by the PNS. What other factors influence gastric motility?

Answer 32

1. Liquids > CHO, > protein > fat
2. Isotonic contents empty faster
3. Fat and H+ SLOW emptying

Question 33

Physio: In the small intestine, the peristaltic reflex acts to allow movement of the bolus down the tube. Describe the peristaltic reflex

Answer 33

1. enterochrommafin-like cells
   - -secrete 5HT
2. Ach, P, Y
   - -contract circular muscle (CM)
   - -longitudinal (LM) relaxes
3. VIP, NO
   - -CM relaxes
   - -LM contracts

Question 34

Physio: A vomiting center in the medulla coordinates the vomiting reflex. Afferent info comes to the vomiting center from the vestibular system, back of the throat, Gi tract, and chemoreceptors.

The vomiting reflex involves reverse peristalsis. Explain

Answer 34

1. Simultaneous contraction of thoracic diaphragm, ab muscles against glottis
   - -relax LES and diaphragm
2. High intraabdominal pressure moves contents into esophagus
3. Breathing muscles contract
   - -inc. thoracic pressure
4. Expulsion of vomit from mouth

NOTE: The UES remains closed with retching; contents return to stomach

*cannabinoid receptors inhibits vomiting center

Question 35

Physio: Salivary secretions are regulated by both the PNS and SNS.

1. The primary NT for the sympathetic nervous system is _______ and it induces secretion of a glycoprotein rich mucous.
2. The primary NT for the parasympathetic nervous system is _______ and it induces secretion of a serous, enzyme rich mucous.

Answer 35

1. Sympathetic:
   - -NE
   * glycoprotein rich mucous
2. Parasympathetic:
   - -Ach
   - -inc. serous, enzyme rich

*dry mouth = dec. parasympathetic
NOTE: salivary secretions inhibited by sleep, dehydration, atropine

Question 36

Physio: Bile functions to emulsify lipids facilitating digestion. It also plays a role in producing micelles that are essential for absorption.

What is the difference between primary bile acids and secondary bile acids?

Answer 36

Primary:

• -cholic/chenodoeoxycholic acid
• -synthesized in liver (from cholesterol)

Secondary:

• -deoxycholic/lithocholic
• -produced via intestinal bacteria

Question 37

Physio: Digested products include FFA, 2-monoglyceride, cholesterol and lysophospholipid. These lipophilic products are absorbed into the cell, re-esterified, and formed into _______ that can leave the cell (exocytosed) and enter lymphatics

Answer 37

chylomicrons

Question 38

Physio:

1. Na and Cl are absorbed in the _____ GI tract
2. K+ is absorbed in the _____ and secreted in the colon
3. HCO3- is absorbed in the ______ and secreted in the ileum
4. Vit. D must be activated in the liver and kidney. Vit. D induces synthesis of ______ protein
5. Lipids are absorbed in the ____
6. Iron absorbed in the

Answer 38

1. Entire GI tract
2. Small intestine
3. Jejunum
4. calbindin protein
5. Jejunum
6. Duodenum

Question 39

Physio: Iron is absorbed as heme or Free iron. It binds to _______ in the cell and is transported in the blood, where it binds to transferrin.

Answer 39

apoferritin

*Fe2+ deficiency MC cause of anemia

NOTE: transferrin (major iron transport protein in circulation - binds Fe3+ form); Ferroportin transports Fe2+

Question 40

Physio: B12 binds to proteins in ingested food. It then binds to ______ protein (haptocorrin) in the stomach, and subsequently binds IF in the SI. It is finally absorbed in the terminal ileum.

Answer 40

R protein (haptocorrin)

*gastrectomy/ilectom =

Question 41

Physio: I cells secrete CCK and S cells secrete secretin.

1. _________ is potentiated by Ach and is associated with acinar cells (IP3, Ca2+). It results in inc. glandular enzymes.
2. _______is potentiated by Ach and #1. It is associated with ductal cells (inc. cAMP) and results in aqueous secretions (HCO3, Na). Stimulated by H+.

Answer 41

1. CCK
   - -I cells
   - -Ach potentiates
   - -Acinar cells: IP3, Ca2+
   - -glands (inc. enzymes)

*Trp, Met, peptides, fa’s

2. Secretin
   - -S cells
   - -Ach and CCK potentiate
   - -Ductal cells: cAMP
   * aqueous secretions (HCO3-, Na)

*H+ stimulates

Question 42

Oral: Orofacial clefts (cleft lip/palate) most often occur in mothers >35 years, alcoholic mothers, and have an increased risk in siblings. What are complications of these clefts?

a. difficulty feeding
b. malocclusion
c. eustachian tube dysfunction
d. speech difficulties

Answer 42

all of the above

*psychosocial

Tx: surgical repair

NOTE: Cleft lip/palate - 50%; alone - 25%

Question 43

Oral: In normal orofacial development, the maxillary processes grow medially, causing the medial nasal processes to be displaced toward the midline. These nasal processes then fuse at the midline. Simultaneously, the palatal shelves fuse in the midline.

What happens in the case of clef lip? cleft palate?

Answer 43

Cleft lip:
–failure of maxillary and medial nasal processes to fuse

Cleft palate:
–failure of palatal shelves to fuse

Question 44

Oral: A 24 year old male presents to the clinic with a mass on his lateral neck. Upon examination, you note a well circumscribed cyst containing clear watery to mucoid debris. The cyst is measured to be 3cm in diameter.

Histology reveals:
1. fibrous walls lined by strat. squ. or pseudostratified epithelium; contains lymph tissue

It is most likely

Answer 44

Branchial cleft cyst

• lateral neck (along sternocleidomastoid)
• remnant of 2nd branchial arch
• ~2-5 cm diameter

Question 45

Oral: A patient presents with a sore throat. She complains she has had a cough and runny nose for the past 2 days. Upon examination, you note erythema and edema of the pharynx with exudate. You also note conjunctivitis.

What is the most common cause for her pharyngitis?

Answer 45

Viral infection

• rhinovirus, adenovirus
• sore throat, runny nose, cough, erythema and edema

Question 46

Oral: A patient presents with white plaques on the lateral tongue. He claims that it is painless, but he cannot scrape it off.

What do you suspect?

Answer 46

Hairy leukoplakia

*EBV reactivation
(immunocompromised)

*confluent, white area on lateral tongue; no pain

Question 47

Oral: Herpes Simplex Virus (1 and 2) can cause oral (and genital) lesions. These viruses initially infect the contacted area, and then travel to the sensory root ganglia where they remain dormant.

True/False: Recurrence occurs when the dormant virus in the ganglia travels back down the nerve to the skin or oral mucosa.

Answer 47

True

• Present as group of vesicles on mucous membranes of lips (herpes labialis) and mouth
• latent: trigeminal ganglia

Question 48

Oral: HSV-1 and HSV-2 infections can have extensive intra-oral mucous membrane involvement.

Cold sores (fever blisters) are a manifestation of recurrent HSV infection that often affects the corners of the mouth. They tend to be less severe, more localized, and of shorter duration than the primary episode. What are triggers for cold sores?

Answer 48

Triggers: Stress, pregnancy, menses, fever, UV light

Question 49

Oral: A 31 year old female presents to the clinic with oral lesions. They appear vesicular that ulcerate. Lab confirms viral infection.

You suspect

Answer 49

Cold sores

*vesicles that ulcerate

Question 50

Oral: A 15 month old presents with a low grade fever, sore throat, and a rash characterized by mildly painful, shallow yellow ulcers surrounded by red halos.

The rash is found on the mucosa of the mouth, palms, feet, and buttocks. What do you suspect?

Answer 50

Hand, Foot and Mouth Disease (Coxsackie)

• shallow, yellow ulcers surrounded by red halos
• labial or buccal mucosa (tongue, soft palate, uvula)
• palmar, plantar, interdigital surfaces of hands and feet; buttocks (maybe)

Question 51

Oral: A 12 month old presents to the clinic with acute onset of high fever (102o) and painful vesicles on the posterior oropharynx (soft palate, tonsils, and uvula). Based on your experience, you know these papular lesions will become fluid-filled vesicles that will eventually rupture forming shallow, painless yellow-gray ulcers.

What is the child presenting with? How is it treated?

Answer 51

Herpangina (Coxsackie)

Tx: Spontaneous resolution

• papules – 1-2mm fluid filled vesicles – rupture to form shallow, yellow gray ulcers
• acute onset high fever (102-104F)

Question 52

Oral: A patient presents with the following:

1. abrupt onset sore throat
2. tonsillar exudate
3. cervical adenopathy
4. fever
5. palatal petechiae

You note her pharyngitis is bacterial. What do you suspect?

Answer 52

Strep pyogenes
(Group A)

Tx: Antibiotics

Question 53

Oral: What are complications of group A strep?

a. acute rheumatic fever
b. peritonsillar abscess
c. cleft palate/lip
d. ludwig’s angina

Answer 53

A and B

• acute rheumatic fever (antibiotics during initial infection)
• peritonsillar abscess (GAS + fusobacterium necrophorum (anerobic))

Question 54

Oral: A patient presents with thrombophlebitis (clotting) of the internal jugular vein. He states he had strep throat when he was younger, but did not receive treatment for it.

Labs indicate an anaerobic bacterium. What do you suspect? What is the outcome?

Answer 54

Lemierre’s syndrome (fusobacterium necrophorum)

Features:

• thrombophlebitis of IJV
• -rare
• -potentially fatal

Question 55

Oral: A patient presents with fever, chills, malaise, drooling, mouth pain and dysphagia.

PMH significant for recent infection of his upper molar (dental).

You suspect Ludwig’s angina, an infection of the submandibular space by the flora of the oral cavity (polymicrobial; viridans). What is a major concern?

Answer 55

Airway obstruction

*monitor and prevent asphyxia

• -aggressive, spread rapidly
• -muffled voice or can’t speak

Question 56

Oral: Cervicofacial actinomycosis involves oral colonization by Actinomyces. It is often introduced into the mucosa by mucosal breach (from infection or trauma). Infection then ensues, forming abscesses and draining sinus tracts.

What are risk factors? Who are most at risk?

Answer 56

RIsk factors:

• -diabetes mellitus
• -immunosuppressed
• -malnutrition

Most at risk: poor oral hygiene

Clinical: slowly progressive mass in the neck/face (mandible region) w/ purulent discharge (sulfurous granules).

Question 57

Oral: A patient presents with a slow growing mandibular mass with purulent discharge containing “sulfur granules”. These granules are yellow aggregates of pus + gram (+) filamentous, anaerobic bacteria.

This best describes?

Answer 57

Cervicofacial actinomycosis

(“sulfur granules”) actinomyces + pus

Question 58

Oral: ______ refers to the localized destruction of teeth by acid-producing plaque bacteria.

This can be prevented by flouridation of water sources.

Answer 58

Dental caries

*flouride incorporated into the enamel = resists degradation

Question 59

Oral: True/False - Although the mechanism is unclear, excess fluoride consumption early in life can cause hypomineralization of the dental enamel.

This can lead to white to brown tooth discoloration

Answer 59

True

**fluoride may directly impair rate of mineral formation

Question 60

Oral: Oral candidiasis is a common local infection known as “thrush”. It is caused by candida albicans (MC). What are the risk factors associated with oral candidiasis?

Answer 60

1. wearing dentures
2. antibiotics
3. immune suppression
4. cellular immune deficiency (AIDS)
5. inhaled corticosteroids

Question 61

Oral: A patient presents with white, curd-like discharge on their tongue (red background). The discharge can be scraped off, leaving a red, raw surface.

Associated symptoms include dysphagia and mouth soreness. What do you suspect?

Answer 61

Thrush (oral candidiasis)

• scrape off = bleeding
• budding yeast and pseudohyphae

Question 62

Oral: _______ refers to one or more small (mm) painful ulcers that are usually on the inner lip or tongue. They are typically seen in kids and adolescents.

*localized, shallow, round - oval ulcers with a gray base.

Answer 62

Recurrent aphthous stomatitis (“Canker sores”)

• recurrences less frequent in childhood
• spontaneous resolution 1-2 wks

Question 63

Oral: The cause for recurrent apthous stomatitis (canker sores) is unknown, however, it is believed to be dysregulation in local cell-mediated immunity.

What are common associations with the development of canker sores? How are they treated?

Answer 63

Associations:

• stress
• trauma
• hormones
• familial

Tx:

• -symptoms (topical corticosteroid/analgesic)
• -avoid salty or acidic foods/juices

Question 64

Oral: Peutz Jeghers syndrome is an autosomal dominant disorder that is characterized by multiple hmartomatous (different tissues) polyps in the GI tract. It is also associated with mucocutaneous pigmentation (hyperpigmented macules) in the mouth, lips and genitalia and poses increased risk of cancers (GI and non-GI).

It is due to a mutation in what gene?

Answer 64

tumor suppressor STK-11

• hamartomatous polyps
• mucocutaneous pigmentation
• cancers (breast, ovarian, other GI cancers)
• Intussusception (telescoping of bowel; currant jelly stools)

Question 65

Oral: Gray-blue lines that form along the junction of the teeth and gums due to lead poisoning

Answer 65

Lead lines

Question 66

Oral: A patient presents with a history of adrenocortical insufficiency. This insufficiency leads to increased production of pro-opiomelanocortin (a prohormone that is cleaved into ACTH, MSH and others).

Elevated levels of MSH stimulate melanin synthesis, leading to hyper-pigmentation. What do you suspect?

Answer 66

Addison’s disease

Question 67

Oral: A patient presents with an enlarged tongue, drooling, and difficulty eating. You note he has difficulty with his speech, and has stridor due to airway obstruction. You suspect

Answer 67

Macroglossia

-drool, speech impairment, airway obstruction

Question 68

Oral: What are common associations with macroglossia?

a. congenital hypothyroidism
b. amyloidosis
c. acromegaly
d. Addison’s disease

Answer 68

A-C

Tx: based on severity (speech therapy; surgical reduction)

Question 69

Physio: What are the features of salivary secretions (compared to plasma)

Answer 69

–alkaline, high K+, hypotonic

Contain: alpha amylase, lingual lipase, mucous, glycoproteins, Igs

Question 70

Physio: Salivary secretions are stimulated by? Inhibited by?

Answer 70

Stimulated: PNS and SNS

Inhibited by: SLeep, dehydration, atropine

Question 71

Physio: Gastric secretions are viscous fluids composed of mucin and HCO3-. What molecules control acid secretion?

Answer 71

Ach, histamine gastrin

Somatostatin = inhibitory

Question 72

Physio: The stomach is composed of Oxyntic glands and pyloric glands. The oxyntic glands have what cells?

Answer 72

Parietal: HCL, IF
Chief: pepsinogen

Question 73

Physio: Venous blood that moves away from the stomach towards the pancreas is known as the

Answer 73

alkaline tide

Question 74

Physio: The pancreas secretes high volumes of bicarb and enzymes, creating an isotonic solution.

What stimulates pancreatic secretions?

Answer 74

1. Secretin – inc. HCO3-
2. CCK – stimulates enzymes
3. Ach – vago-vagal

NOTE: Acinar cells - CL-; Ductal cells - HCO3-

“secret ducts” = secretin/ductal cells

Question 75

Physio: Crypt cells of the Small Intestine are responsible for secreting Chloride via NKCC in the basolateral membrane. Na entry drives the K+ and Cl- entry. Cl- is then secreted by CFTR into the lumen.

True/False - Luminal Cl- pulls Na and H2O, creating isotonic secretions

Answer 75

True

**cAMP opens Chloride channel (via G alpha protein)

Question 76

Imaging: Achalasia is a disorder characterized by failure of the LES to relax during swallowing. It often presents with dysphagia (hard to swallow) for solids and liquids, regurgitation of food, retrosternal chest pain, and weight loss.

What is a characteristic finding on imagin?

Answer 76

“bird’s beak” sign

• proximal esophageal dilation; narrowing at gastro-esophageal junction
• degeneration of inhibitory neurons

NOTE: Chagas can cause secondary achalasia

Question 77

Imaging:

1. The fundus of the stomach is supplied by ____
2. The lesser curvature is supplied by _____
3. The greater curvature is supplied by
4. This region of the SI has the thickest plicae circulares

Answer 77

1. short gastric arteries
2. left and right gastric
3. L and R gastro-omental
4. jejunum

Question 78

Imaging: There are 4 anatomical parts of the duodenum:

1. Superior
2. Descending
3. Inferior
4. Ascending

What are their features?

Answer 78

1. Superior
   - -L1
   - -mobile, intraperitoneal
2. Descending
   - -L1-L3
   - -pancreatic and common bile empty here (Vater)
3. Inferior
   - -horizontal
   - -L3
4. Ascending
   - -L2 (superiorly)
   - -terminates at duodenal-jejnual flexure

Question 79

Imaging: What happens when there is a mass in the pancreatic head (closeley associated with the duodenum)?

Answer 79

Jaundice

–due to obstruction of distal pancreatic and distal common bile ducts. No bile will enter the duodenum

Question 80

Imaging: Repeated injuty to the pancreas (e.g. alcohol abuse) can cause chronic pancreatitis. This results in destruction of the exocrine cells, and thus, loss of pancreatic enzymes. What is the significance of this?

Answer 80

• malabsorption (enzymes aren’t available to digest fat)

clinical: steatorrhea (greasy stool), secondary diabetes

Question 81

Imaging: A small bowel obstruction can be indicated by the presence of

Answer 81

1. plicae circularis on imaging
2. SI more centrally located
   * *dilated, air filled loops of bowel arranged in a step-wise fashion

*large bowel: haustra do not span the entire bowel; peripherally located

Question 82

Imaging: You receive imaging of a patient.

Imaging reveals circumferential tumor growth with focal constriction and dilation of the colon proximal to the constriction. “Apple core” sign is present.

What does this indicate?

Answer 82

• colorectal cancer
• circumferential tumor growth = focal constriction and dilation of the colon proximal to the constriction

NOTE: must be done with barium

Question 83

Imaging: Diverticulosis is caused by small outpouchings (diverticula) of the colonic wall due to increased intraluminal pressure.

Although usually asymptomatic, what are 2 major complications associated with diverticulosis?

Answer 83

1. Diverticulitis
   - -infection/inflammation
   - -pain L lower quadrant, fever, nausea, vomiting, diarrhea or constipation
2. Bleeding
   - -MC cause of massive lower GI bleeding

Question 84

Imaging: A patient presents with periumbilical pain. You perform several tests, and note rebound tenderness.

Clinical examination reveals pain over McBurney’s point (2/3 b/t umbilicus and ASIS) and a positive Rovsing’s sign (pain in right iliac fossa during palpation of left). You suspect appendicitis. What imaging would you perform? What do you look for?

Answer 84

Imaging: MRI, CT, US

Features: dilated tubular structure, thickened wall, fat standing

Question 85

Imaging: The thoracic aorta exits the aortic hiatus at T12 to become the abdominal aorta. The abdominal aorta gives off multiple branches including

Answer 85

• celiac (T12)
• superior mesenteric (L1)
• inferior mesenteric (L3)
• renal artery
• common iliac arteries (L4)

Question 86

Imaging: List the 5 major veins that contribute to the IVC

Answer 86

1. Common iliac (L5)
2. Lumbar (L1-L5)
3. Right gonadal (L2)
4. Renal (L1)
5. Hepatic (T8)

Question 87

Imaging: It is common to do a full CT exam on patients who experience trauma. What is the first thing that should be assessed?

Answer 87

Integrity of the aorta

Question 88

Imaging: The branches of the celiac artery (T12) include:

1. Left gastric
2. Common hepatic
3. Splenic

What do they supply?

Answer 88

1. Left gastric: stomach, esophagus
2. Common hepatic: liver, stomach, duodenum
3. Splenic: spleen, pancreas, short gastric arteries

Question 89

Imaging: The branches of the Superior Mesenteric Artery include:

1. Inferior pancreaticoduodenal artery
2. Intestinal arteries
3. Ileocolic arteries
4. Right colic artery
5. Middle colic artery

What do they supply?

Answer 89

1. Inferior pancreaticoduodenal: head of pancreas, duodenum
2. Intestinal arteries: Ileum, jejunum
3. Ileocolic: terminal ileum, cecum, appendix
4. Right colic: ascending colon
5. Middle colic: transverse colon

Question 90

Imaging: The branches of the Inferior Mesenteric artery include:

1. Left colic
2. Sigmoid
3. Superior rectal

What do they supply?

Answer 90

1. Left colic: descending colon
2. Sigmoid: sigmoid colon
3. Superior rectal: terminal branch of IMA

Question 91

Imaging: The GI tract is embryologically divided into

1. foregut
2. midgut
3. hindgut

What is the blood supply/boundaries of these divisions?

Answer 91

1. FOregut
   - -celiac
   - -lower esophagus to major duodenal papilla
2. Midgut
   - -SMA
   - -duodenal papilla – 2/3 transverse colon
3. Hindgut
   - -IMA
   - -2/3 transverse to upper anal canal

Question 92

Imaging: The spleen is deep to ribs 9, 10 and 11.

True/False - the spleen has a very thin capsule. This is prone to rupture due to trauma such as a rib fracture

Answer 92

True

*splenic artery supplies spleen - rapid blood loss into peritoneal cavity

Question 93

Imaging: A patient presents with LUQ pain and tenderness. You note bruising on ribs 9 and 10, confusion and dizziness. The patient is hypotensive due to extensive blood loss. What do you suspect?

Answer 93

Splenic rupture

Question 94

Imaging: A patient presents complaining of shoulder pain and pleuritic chest pain. You notice she is breathing deeply. She states that she eats less than normal because she always feels full. On palpation, you note the spleen can be felt. What do you suspect?

Answer 94

Splenomegaly

• fullness, referred shoulder pain, difficulty breathing
• Risk factors: Mono (EBV), Hematological malignancy, portal HTN, malaria

Question 95

Imaging: True/False - A spleen is not palpable until it is 3x its normal size

Answer 95

False

2x its normal size

Question 96

Imaging: The tail of the pancreas lies in close proximity to the splenic hilum and is supplied by branches of the splenic artery.

True/False - the pancreatic tail is prone to iatrogenic injury during splenectomy when the hilum and vessels are clamped

Answer 96

true

Question 97

Imaging: The gallbladder stores and concentrates bile before it is released into the SI. When components of bile become concentrated beyond the point of solubility, the precipitate to form gallstones.

What are the types of gallstones? which is most common?

Answer 97

1. Cholesterol (80%)
2. Bilirubin (chronic hemolysis)
3. Pigment (bilirubin stones via oxidation)

Question 98

Imaging: Blood flow from the spleen and GI tract is delivered to the liver through the portal vein (superior mesenteric + splenic veins).

What are the consequences of portal HTN?

Answer 98

1. ascites (fluid in peritoneal cavity)
2. Splenomegaly (lead to thrombocytopenia)
3. Esophageal varices (dilated veins – hematamesis)
4. Caput medusae (dilated peri-umbilical collateral veins)

Question 99

Imaging: True/False - repeated injury to the liver (alcohol, chornic viral hepatitis) can cause irreversible damage (cirrhosis)

Answer 99

true

Question 100

Oral: Inflammatory disorder of the tongue that leads to atrophy of the filiform papilla. The tongue will appear smooth, glossy and erythematous. MC due to nutritional deficits (Fe, B12, folate).

Answer 100

Atrophic glossitis

due to: nutritional deficiencies (Fe, B12, folate); Sjogren; oral candidiasis, protein-calories malnutrition elderly

Question 101

Oral: A patient presents complaining of burning sensation in her mouth along with increased sensitivity when she eats acidic and/or salty foods. You note that her tongue appears smooth, glossy and erythematous. You suspect? How would you treat?

Answer 101

atrophic glossitis

Tx: correct underlying condition

Question 102

Oral: Drug induced-gingival overgrowth is believed to be due to a direct effect of a drug combined with inflammatory changes induced by bacteria. With which drugs is it most often associated?

a. phenytoin
b. Isoniazid
c. cyclosporine
d. Ca2+ channel blockers

Answer 102

Answer: Phenytoin (anti-epileptic), Cyclosporine, Ca2+ blockers

• severity/distribution: dose and case specific
• may interfere with hygiene and impair chewing

Question 103

Oral: A clinical term used to describe an asymptomatic “white plaque” that CANNOT be scraped off. It has low risk of dysplasia/malignancy.

Answer 103

Leukoplakia

Dx: must biopsy

Note: multifactorial (tobacco MC);
–inner lip, floor of mouth

Question 104

Oral: A clinical term for “red plaque”. It is more likely to represent a dysplastic or malignant process.

Risk factors include: Tobacco (MCC), OH, and HPV.

Answer 104

Erythroplakia

• -red color due to subepithelial vascular dilation
• *Tobacco

Dx: Must biopsy to rule out squamous dysplasia/cancer

Question 105

Oral: _______ is a benign tumor located in the mandible. It arises from teeth-forming (odontogenic) epithelium.

Imaging reveals radiolucency of the bone (“soap bubble”).

a. pyogenic granuloma
b. ameloblastoma
c. squamous cell carcinoma of the mouth
d. papillary adenoma

Answer 105

Ameloblastoma

• arises from teeth-forming (odontogenic) epithelium
• locally invasive; does NOT metastasize

Question 106

Oral: Squamous cell carcinoma is the MC malignancy of the oral cavity. Risk factors include:

1. tobacco
2. alcohol
3. HPV (16)
4. sunlight (lower lip)

What are the MC sites?

Answer 106

1. lower lip (vermillion border)
2. floor of mouth
3. lateral tongue

Question 107

Oral: A 9 year old presents to the clinic with a benign tumor of the oral cavity.

On PE you note the tumor is present on the gingiva.

Histology reveals:
1. lobules of capillary-sized vessels (lobular capillary hemangioma)

You suspect

a. choriocarcinoma
b. nevus simplex
c. pyogenic granuloma
d. hemangioma

Answer 107

Pyogenic granuloma (benign prolif. of small vessels)

• MC kids and young adults
• MC gingiva, maybe lips, buccal mucosa, tongue

Question 108

Oral: Kaposi sarcoma is a malignant neoplasm of endothelial cells. It is most often associated with HHV-8. It involves the mucous membranes, skin and viscera of the GI tract.

What are the 4 epidemiologic forms?

Answer 108

1. AIDS associated
   - -AIDS defining
   - -MC AIDS malignancy
2. Transplant - associated
   - -T-cell immunosuppression (solid organ)
3. Classic (sporadic)
   - -elderly males; Mediterranean descent
4. Endemic African
   - -HIV seronegative

Question 109

Oral: __________ is caused by autoimmune destruction of the exocrine glands (including lacrimal and salivary glands). It is most often seen in middle aged females.

Answer 109

Sjogren syndrome

-lymphocytic inflammation/destruction of exocrine glands that results in fibrosis

Question 110

Oral: A 45 year old female presents with complaints of dry eyes and dry mouth. She reports gritty, sand-like feeling in her eyes. Patient admits to difficulty swallowing dry foods such as crackers.

On PE you note enlargement of the salivary glands (sialadenitis).

Labs reveal:

1. Anti-SSA (+)
2. Anti-SSB (+)

You suspect

Answer 110

Sjogren syndrome

1. Dry eyes
   –keratoconjunctivitis sicca, xeropthalmia
   (gritty feeling/sand in eyes)
2. Dry mouth
   - -xerostomia (difficulty swallowing dry food; crackers)
3. Salivary gland enlargement
   - -sialadenitis (inflammation)

Question 111

Oral: Sjogren syndrome is caused by autoimmune destruction fo the exocrine glands (including lacrimal and salivary glands). It is most often seen in middle aged females.

Describe associated complications. How is it diagnosed?

Answer 111

Complications:
–inc. risk dental caries, lymphoma

Dx: Anti-Ro (SSA) and anti-La (SSB-autoabs)

Question 112

Oral: A patient presents with complaints of oral pain and swelling.

On PE you note the presence of a stone in the salivary duct (Wharton’s duct - MC). Skin tenting present.

You suspect

Answer 112

Sialolithiasis

MC - Wharton’s duct (drains submandibular gland)

RIsk factors:
-dehydration (e.g. Sjogren), meds that dec. salivary production (anti-cholinergics)

Question 113

Oral: Sialadenitis is characterized by inflammation of the salivary glands. Associated symptoms are firmness, pain and swelling.

It most often involves either the parotid or submandibular gland. What are common causes?

Answer 113

1. Sjogren’s
2. Mumps (bilateral)
3. Duct obstruction (unilateral)
   - -Staph aureus
   - -dehydration

Question 114

Oral: A pseudocyst of the minor salivary gland. It is formed when the salivary gland duct is blocked or ruptured (secondary to trauma – biting lip or cheek).

Answer 114

Mucocele

• secretions will dissect into the soft tissues (around the gland)
• pooling of mucous

Question 115

Oral: A patient presents with painless swelling of the lower lip/buccal mucosa. You note a translucent/bluish “cyst” < 1cm on her inner lip.

What do you suspect? How do you treat?

Answer 115

Mucocele

• painless swelling
• translucent or bluish

Tx: resolves spontaneously or excise

Question 116

Oral: Salivary gland neoplasms that occur in the parotid gland (MC) are rare and mostly benign. They will often present as a painless mass.

What features could indicate malignancy?

Answer 116

1. tumors in the other salivary glands
2. **neurologic signs (facial nerve paralysis) **
3. radiation exposure (inc. risk)

Question 117

Oral: Parotid tumors drain into ____ lymph nodes first, then to the upper cervical nodes

Answer 117

intra-parotid lymph nodes

Question 118

Oral: A patient presents with a painless, slow growing, mobile mass at jaw angle

Biopsy reveals a “benign mixed tumor” that exhibits epithelial and mesenchymal differentiation.

Answer 118

pleomorphic adenoma

RF’S:

1. MC females
2. Radiation exposure (15-20 yrs. later)
3. Recurrence (if incompletely excised)

• low risk of malignant transformation
• MC parotid gland

Question 119

Oral: A patient presents to the clinic with a mass on his face along the parotid gland. He states that it is painless, but it seems to be growing larger.

1. Social history: Smoker for 20 years
2. Histology: double layer of palisading neoplastic columnar and cuboidal epithelial cells resting on a dense lymphoiod stroma (w/ germinal centers)

What do you suspect?

Answer 119

Warthin tumor

• MC males
• MC smoking
• Parotid ONLY
• no malignant change

Question 120

Oral: ________ is the MC primary malignant tumor of salivary glands. It is composed of an admixture of 3 cell types:

• mucocytes
• epidermoid cells
• intermediate cells

It most often occurs in the parotid gland and can be low, intermediate or high grade depending on the degree of anaplasia.

Answer 120

Mucoepidermoid carcinoma

Clinical course and prognosis depend on the grade.

Question 121

Oral: Adenoid cystic carcinoma is a relatively uncommon and slow growing salivary gland tumor. It is aggressive and has a propensity for ____ invasion.

Typically, prognosis is poor (risk of distant metastasis years later).

Answer 121

perineural

Question 122

PUD drugs: _________ primarily act to neutralize acid secreted in the stomach. They provide subsequent mucosa protection

Answer 122

Antacids

Question 123

PUD drugs: _____ protect any area of the GI system from further damage and/or promote recovery

Answer 123

Mucosa protectants

Question 124

PUD drugs: _____ block/reduce gastric acid secretion

Answer 124

H2 antagonists and protein pump inhibitors

*H2 antags = first line Tx for peptic ulcers

Question 125

PUD drugs: Treat H. pylori

Answer 125

Antibiotics

Question 126

PUD: Antacids act to:

1. Neutralize the acid secreted in the stomach.
   - -formulations include Na, Ca, Al or Mg ions.
2. Decrease tissue injury by maintaining the pH at ~5 (reducing pepsin activity).
3. Decrease acidity and aid with headache
   - -buffered antacid (alka-seltzer) - aspirin + NaHCO3 + citric acid

What do antacids NOT do?

Answer 126

• do not prevent acid production

- do not coat the lining of peptic ulcers or GI mucosa

Question 127

PUD: What are the adverse effects of the following antacids?

1. NAHCO3 (high neutralizing capacity)
2. CaCO3 (moderate)
3. Al(OH3) (high)
4. Mg(OH2) (high)

Answer 127

1. NaHCO3
   - -short, fast effects
   - -systemic alkalosis
2. CaCO3
   - -moderate
   - -hypercalcemia; inc. gastrin; acid rebound
3. AlOH3
   - -Constipation
4. Mg
   - -diarrhea
   - –hyperMg (renal insufficiency)

Question 128

PUD: Which of the following is a drug interaction of Antacids?

a. decrease absorption of acidic drugs (e.g. phenytoin)
b. form insolbule chelate complexes w/ antibiotics
c. decrease cimetidine bioavailability

Answer 128

All of the above

1. decrease absorption of acidic drugs
   - –digoxin, phenytoin, chlorpromazine) = decrease their efficacy.
2. chelate complexes
   - -tetracyclines and fluouroquinolones
   - -take 4 hours before (or 2 hrs. after antibiotic)
3. decrease cimetidine bioavailability
   - -take drugs apart

Question 129

PUD: What is a contraindication for antacids?

Answer 129

renal failure (hypermagnasemia, AI toxicity)

Question 130

PUD: Mucosal protectants are used to treat stomach, duodenal, and esophageal ulcers (less efficiently than H2 antagonists and PPI’s).

Examples of these drugs include:

1. Bismuth salicylate
2. Sucralfate
3. Misoprostol

_____relieves heartburn, nausea and diarrhea. It limits acid secretion in the GIT, and inhibits H. pylori.

Answer 130

Bismuth

*anti-inflammatory effect (salicylic acid)

NOTE:
-poorly absorbed
Adverse: black stools
Cx: bleeding with ulcers

Question 131

PUD: Mucosal protectants are used to treat stomach, duodenal, and esophageal ulcers (less efficiently than H2 antagonists and PPI’s).

Examples of these drugs include:

1. Bismuth salicylate
2. Sucralfate
3. Misoprostol

_____ prevents ulcers produced by NSAIDS.

Answer 131

Sucralfate

NOTE:

• -local effect
• -Adverse: Constipation, dry mouth
• -Cx: hypophasphatemia; renal dysfxn

Question 132

PUD: Which of the following are mechanisms of action of sucralfate?

a. interacts with proteins at the ulcer site to form a protective layer
b. prevents acid exposure and promotes faster healing
c. inhibits pepsin = dec. tissue injury
d. binds bile salts to protect the stomach lining (from bile acid)

Answer 132

All of the above

Also:
-Inc. PG secretion: restitution and preservation of gastric mucosa

-Suppress H. pylor infection

Question 133

PUD: Mucosal protectants are used to treat stomach, duodenal, and esophageal ulcers (less efficiently than H2 antagonists and PPI’s).

Examples of these drugs include:

1. Bismuth salicylate
2. Sucralfate
3. Misoprostol

____ is a PGE1 analog that is used (rarely) for the prevention and treatment of ulcers produced by NSAIDS. It acts to protect the mucosa by increasing HCO3- and mucous secretion.

Answer 133

Misoprostol

Adverse: Diarrhea
Cx: Pregnancy (miscarriages; birth defects)

Question 134

PUD: List the drug interactions of mucosa protectants

1. Bismuth salicylate
2. Mg antacids and misoprostol
3. Sucralfate

Answer 134

1. Bismuth
   - -dec. absorption of tetracyclines
2. Mg antacids and misoprostol
   - -inc. diarrhea (Mg)
3. Sucralfate
   a. decreases efficacy of azole anti-fungals, cimetidine, digoxin
   b. if px takes Lansoprazole, administer 30 min apart (it inhibits sucralfate absorption)

Question 135

PUD: H2 antgonists act to inhibit gastric acid secretion and stimulate mucous synthesis/secretion. They are more often used when other treatments fail.

What is their mechanism of action?

Answer 135

–inhibit H2 receptors (dec. HCl production)

• inhibit both meal and basal acid secretions
• Clinical use: Zollinger, GERD, H. pylori

Question 136

PUD: H2 antagonists include Cimetidine, Famotidine and Nizatidine. Of the 3, Famotidine has the longest duration and is the most potent.

What are side effects of these drugs?

Answer 136

1. Common
   - -diarrhea, headache, constipation, nausea
2. Long term (high dose)
   a. cimetidine: inhbits DHT = gynecomastia (men); galactorrhea (women)

Question 137

PUD: List the drug interactions associated with H2 antagonists

Answer 137

1. Prevent PPI activity
   - -take 4 hrs apart
2. Dec. absorption of azoles, iron, cyclosporine
3. Cimitedine inhibits CYP450 (dec. drug metabolism; inc. side effects)
   - -warfarin, tricyclic anti-depressants, anti-convulsants

Question 138

PUD: Proton Pump Inhibitors (PPI’s) are most effective for the treatment of GERD. Their efficacy is similar to H2 antagaonists (for PUD).

They can be used to treat Zollinger-Ellison at higher doses, and can be used in combo with clarithromycin for H. pylor infections. What is the MOA of PPI’s?

Answer 138

1. prodrug – reactive agent (in parietal cell lumen)

- -covalently attach to the H+/K+ ATPase

Question 139

PUD: Omeprazole (Prilosec) and Esomeprazole are types of PPI’s. Omeprazole is the racemic mix (inactive R+ isomer) that gets converted in the liver to esomeprazole (enantiomer) by CYP2C19.

It has lower efficacy in “poor metabolizers”. How does this differ from Esomeprazole (Nexium)?

Answer 139

Esomeprazole = same conc. for normal and poor metabolizers

Question 140

PUD: To be effective, PPI’s should be taken 30 minutes before eating. Which PPI has the highest, fastest activity? Which has the highest bioavailability?

Answer 140

1. Fastest activity
   - -Rabeprazole
   * 5 minutes to inhibit
2. Greatest bioavailability
   - -Lansoprazole

Question 141

PUD: PPI’s are normally well tolerated, however, the longer the exposure, the greater the risk of adverse effects.

Which of the following is a common adverse effect of PPI’s?

a. Headache, diarrhea, abdominal pain, nausea and vomiting
b. Inc. gastrin secretion – mucosal hyperplasia
c. Increased risk of bone fractures (dec. Mg)

Answer 141

All of the above

Question 142

PUD: True/False - PPI’s have pH dependent drug interactions. The decreased acidity in the stomach (long term) can cause decreased absorption of ketoconazole, aspirin, and atazanivir. Furthermore, they can cause decreased absorption of ions including Ca2+, Magnesium and Vit. B12.

Answer 142

True

Question 143

PUD: PPI’s can have pH- independent interactions. For example, Omeprazole/esomeprazole inhibit the metabolism (2C19, 2D6, and 3A4) of warfarin, diazepam and phenytoin, increasing drug activity and side effects.

What effects do they have with anti-platelet drugs?

Answer 143

Dec. anti-platelet activity of clopidogrel

Question 144

PUD: True/False - PPI’s Pantoprazole/Rabeprazole have less inhibitory effects on CYP enzymes, and thus have no significant drug interactions.

Answer 144

True

Question 145

PUD: 80-95% of patients with ulcers have an H. pylor infection. Typically treatment involves a multi-drug therapy:

1. Begin Tx with acid reducing agent (H2 or PPI for 6wks)
2. Next Tx with 2 or ore antibiotics or bismuth (2wks)

12-month remission rates are higher after successful eradication. What are combined drugs used to Tx H. pylori?

Answer 145

1. Lansoprazole (omeprazole) + amoxicillin and clarithromycin
2. Omeprazole + amoxicillin + rifabutin
   - -if H. pylori is resistant to clarythromycin and metronidazole
   - -higher eradication

Question 146

PUD: For the following antibiotics, list the side effects, drug interactions and contraindications

1. Clarithromycin
2. Amoxicillin
3. Metronidazole
4. Tetracycline
5. Omeprazole + Amox + Rifambu

Answer 146

See table in Notes

Question 147

Esophageal: A mother presents to the clinic with her 3 week old infant. She reports he has been drooling, choking and spitting up after feeding.

On PE you note polyhydramnios.

Catheter placement fails (cannot pass further than ~10-15cm).

A-P CXR reveals catheter curls in the upper esophageal pouch.

You suspect

Answer 147

Tracheoesophageal fistula

• MC congenital abrnomality of the esophagus
• abnormal connection b/t trachea and esophagus

NOTE: associated with VACTERL: vertebral anomaly, anal atresia, CV defects, TE fistula, renal issues, limb issues

NOTE 2: MC fistula b/t distal trachea and esophagus

Question 148

Esophageal: A ring of mucosal prominence in the upper esophagus. It is Idiopathic and often asymptomatic.

Clinical include dysphagia for solid food.

Answer 148

Esphageal web

MC - women > 40

NOTE: Seen in Plummer Vinson syndrome (web, Fe anemia, beefy red tongue)

Question 149

Esophageal: How does esophageal web differ from Schatzki’s ring?

Answer 149

Schatzki’s is in the lower esophagus

*circumferential and symptomatic

Question 150

Esophageal: Refers to herniation of abdominal tissues through the esophageal hiatus of the diaphragm. It is usually asymptomatic, but can increase the risk of reflux (GERD).

Answer 150

Hiatal hernia

• unknown etiology - inc. abdominal pressure (pregnancy, obesity, ascites)
• usually acquired

NOTE: may present with epigastric pain, early satiety, GERD/retching

Question 151

Esophageal: With regard to hiatal hernias, most are asymptomatic. However, larger ones can increase the risk of GERD.

True/False: Surgical repair is usually reserved for symptomatic patients and for management of complications (obstruction, strangulation, perforation)

Answer 151

True

• NOTE: sliding hiatal hernia (defect in diaphragm - stomach slides up into chest)
• NOTE 2: parasophageal hiatal hernia (proximal stomach – adjacent to esophagus = strangulation)

Question 152

Esophageal: The esophagus functions as a pump, the LES as a valve and the stomach as a reservoir.

Gastroesophageal reflux may occur as a result of:

a. absent esophageal peristalsis (e.g. achalasia, scleroderma)
b. dysfunctional LES
c. delayed gastric emptying

Answer 152

All of the above

a. absent esophageal peristalsis
- –achalasia, scleroderma (dec. clearance of acidic material)

b. dysfunctional LES
- -hiatal hernia, anti-cholinergic, fatty food, nicotine (reflux of gastric contents)

c. delayed gastric emptying
- -gastroparesis (inc. gastric volume and pressure overwhelms LES –GERD)

Question 153

Esophageal: Gastroesophageal reflux disease can be due to decreased LES pressure, and increased intra-abdominal pressure. This leads to backflow of gastric contents (acid and bile) into the lower esophagus.

What are common etiologies leading to decreased LES pressure?

Answer 153

• progesterone (pregnancy)
• coffee
• alcohol
• smoking (nicotine)
• chocolate
• fatty foods
• medications (Ca2+ channel blockers, anti-Achs)

NOTE: stomach contents flow back into the esophagus causing irritation of the mucosa. Due to innappropriate, transient relaxation of the LES.

Question 154

Esophageal: Gastroesophageal reflux disease can be due to decreased LES pressure, and increased intra-abdominal pressure. This leads to backflow of gastric contents (acid and bile) into the lower esophagus.

What are common etiologies leading to intra-abdominal pressure?

Answer 154

• coughing
• straining (valsalva)
• bending

Question 155

Esophageal: A 32 year old female presents complaining of heartburn (retrosternal burning sensation), chest pain and regurgitation.

What do you suspect?

Answer 155

GERD

Question 156

Esophageal: Complications of GERD include

1. Reflux esophagitis
2. bleeding
3. stricture
4. Barrett esophagus – CA

______ occurs when refluxed gastric acid and pepsin cause necrosiss of the esophageal mucosa that presents with erosions/ulcers

Answer 156

Reflux esophagitis

Question 157

Esophageal: Treatment for gastroesophageal reflux disease includes:

1. lifestyle changes
2. medications
3. surgical

List examples of lifestyle changes

Answer 157

1. elevate head with blocks
2. reduce meal size
3. don’t eat immediately before bedtime
4. weight loss (if overweight)
5. if smoker: quit smoking
6. avoid aggravating food, drinks, meds

Question 158

Esophageal: Treatment for gastroesophageal reflux disease includes:

1. lifestyle changes
2. medications
3. surgical

List examples of Medications and Surgical

Answer 158

Meds:
–H2 antagonists, antacids, PPI’s (omeprazole)

Surgical:
–Nissen fundoplication
(proximal stomach wrapped around distal esophagus to create anti-reflux barrier

Question 159

Esophageal: Barrett’s esophagus results from chronic irritation of the distal esophagus that leads to intestinal metaplasia.

Describe this histological change

Answer 159

1. Squamous epithelium to columnar w/ goblet cells
2. Salmon colored mucosa

• predominantly white males
• inc. risk dysplasia/malignancy

Question 160

Esophageal: A 38 year old HIV (+) male presents with complaints of odynophagia (pain with swallowing), dsyphagia, and chest pain. He has a CD 4 < 100 .

You suspect

Answer 160

Infectious esophagitis

*immunocomp, transplant px

NOTE: odynophagia - uncommon in reflux

Question 161

Esophageal: A patient presents to the clinic with odynophagia (pain swallowing) and dysphagia (difficulty swallowing). You note white plaques with friability that bleed when scraped.

Labs indicate a budding yeast with pseudohyphae. What do you suspect? In what patients is this MC?

Answer 161

Candida esophagitis

• -odyno and dysphagia
• -friable white plaques

Patients: AIDS (AiDS defining), chemo/radiation, transplant, esophageal stasis (achalasia, strictures, scleroderma)

Question 162

Esophageal: HSV 1 and 2 can cause HSV esophagitis. It typically presents in patients who are immunocompromised.

Signs and Symptoms include vesicles on their lips, odynophagia and dysphagia.

Describe their clinical appearance

Answer 162

Multiple, discreet “punched out” ulcers

*viral cytopathic effect: nuclear inclusions

Question 163

Esophageal: CMV esophagitis presents with “serpiginous ulcers” in otherwise normal mucosa.

It most often occurs in what patients?

Answer 163

• immunocompromised
• organ transplant on immunosuppressive therapy

*viral cytopathic effect = nuclear and cytoplasmic inclusions

Question 164

Esophageal: Increased intra-epithelial eosinophils in the absence of other known causes + dysphagia and food impaction describes

Answer 164

eosinophilic esophagitis

• young, white males
• Hx: food allergy, asthma, eczema, allergic rhinitis

Question 165

Esophageal: What are characteristic histologic and clinical features of eosinophilic esophagitis?

Answer 165

1. concentric mucosal rings (endoscopy)

2. innumerable eosinophils (biopsy)

Question 166

Esophageal: Pill esophagitis refers to the development of erosions and or ulcers at the site where medication lodges (in esophageal lumen). Symptoms include chest pain and odynophagia. It may heal with scarring causing stricture.

What are pre-disposing factors?

Answer 166

Features:
–discrete ulcer with normal appearaing background mucosa

Pre-disposing:

• -inadequate liquid intake w/ pill (dry swallow)
• -recumbent position soon after ingestion

Question 167

Esophageal: What are the MC medications associated with pill esophagitis?

a. NSAIDs, Bisphosphonates, Tetracyclines, Supplements
b. Anticholinergics, Bisphosphonates, Fluoroquinolones, Tetracyclines
c. ACE inhibitors, tetracyclines, NSAIDs, B-blockers

Answer 167

A

NSAIDs (ASA)
Bisphosphonates
Tetracylines
K+ and Fe2+ supplements

Question 168

Esophageal: Achalasia is an uncommon disorder with unknown etiology. Evidence suggests an autoimmune response triggered by HSV-1.

It occurs equally in males and females between the ages of 25-60. Regardless of the underlying cause, there tends to be a lack of what within the esophagus?

Answer 168

lack inhibitory ganglion cells within the esophagus

Question 169

Esophageal: A patient presents with difficulty swallowing (dysphagia) both liquids and solid foods.

You perform a barium swallow and esophageal manometry. Results reveal a dilated esophagus with air fluid level. “Bird beak” sign is noted.

You are concerned of his risk of aspiration because you suspect

Answer 169

Achalasia

• lack of esophageal peristalsis
• failure of the LES to relax during swallowing.

Question 170

Esophageal: Chagas disease is an acquired cause of achalasia. It is due to infection by Trypanosoma cruzi. Although infection is lifelong, only a small minority develop serious problems.

What is the pathogenesis of Chagas?

Answer 170

–chronic low levels of parasites in tissues = chronic inflammation = pathologic changes

Question 171

Esophageal: Chronic infection by T. cruzi is most likely to cause myocarditis. It may also involve the esophagus and colon, causing a loss of ganglion cells (leading to dilation).

What are the clinical manifestations?

Answer 171

–similar to achalasia (dysphagia initially to solids, eventually liquids)

-Romana’s sign: unilateral swelling of eyelid
(inflammation at inoculation site)

*megaesophagus, megacolon

Question 172

Esophageal: Esophageal strictures are most often caused by

Answer 172

1. Reflux esophagitis (MC)
2. corrosive esophagitis - alkali or acid
3. Iatrogenic, Pill esophagitis, Radiation esophagitis, Malignancy

Question 173

Esophageal: Esophageal strictures most commonly present with dysphagia (solids). This may be progressive, but is not intermittent.

How is it treated? What are potential complications?

Answer 173

Tx:
-esophageal dilatation (may have to be repeated)

Complications:

• -chronic relapsing course
• -inc. risk of food impaction, aspiration
• -inc. risk of perforation
• -dilatation may need to be repeated

Question 174

Esophageal: A diverticulum describes outpouching of the wall of a tubular organ.

1. _______: indicates presence at birth
2. ______: indicates development later in life
3. ______: incolves all layers of the wall
4. ______: herniation of mucosa and submucosa (through a defect in the muscular wall)

Answer 174

1. Congenital diverticula
2. Acquired diverticula
3. True diverticula
4. False diverticula

Question 175

Esophageal: A diverticulum describes outpouching of the wall of a tubular organ.

1. _____: high intra-luminal pressure pushing out against an area of weakness
2. _____: pulling forces (e.g. traction) on the outside of the esophagus from an adjacent inflammatory process

Answer 175

1. Pulsion diverticula

2. Traction diverticula

Question 176

Esophageal:________ describes an uncommon, false diverticulum that arises immediately above the upper esophageal sphincter.

It is an acquired defect due to stenosis of the cricopharyngus muscle (UES) that leads to obstruction and increased intra-luminal pressure proximally.

Answer 176

Zenker diverticulum

• patients > 60y/o
• can enlarge – accumulate food (regurgitation, halitosis)

Complications: Aspiration pneumonia
Tx: Surgery

Question 177

Esophageal: Midesophageal diverticulum is formed as a result of what?

Answer 177

Traction

• -adjacent inflammatory process
• -asymptomatic but can enlarge and cause issues

Question 178

Esophageal: Describe venous drainage that causes varices

1. Blood flow through the _____ is obstructed (e.g. cirrhosis)
2. Blood flow diverts thorugh the _______ into the esophageal veins
3. Results in abnormally dilated veins of the distal esophagus (a.k.a. varices)

Answer 178

1. portal vein obstruction
2. diverted through the left gastric to esophageal veins
3. dilated distal esophageal veins (varices)

Question 179

Esophageal: Esophageal varices are due to increased pressure or blood flow that results in dilated, tortuous vessels.

What is a complication?

Answer 179

–rupture with massive hematemesis (painless)

• high mortality
• major cause of cirrhosis-related morbidity and mortality

Question 180

Esophageal: A linear mucosal laceration (tear) in the distal esophagus/proximal stomach. It is due to a rapid, large increase in gastric pressure.

It presents with severe vomiting/retching episode followed by hematamesis.

Answer 180

Mallory Weiss tear

• excessive OH or bulemia
• inc. gastric pressure = inc. pressure gradient across GE junction

Question 181

Esophageal: ______ describes spontaneous perforation of the esophagus. It MC occurs from a sudden increase in intra-esophageal pressure caused by vomiting.

Answer 181

Boerhaave syndrome

Iatrogenic: endoscopic perforation MC

Question 182

Esophageal: A patient presents with sudden onset of severe retrosternal (chest) pain and upper abdominal pain that radiates to the back. Patient admits pain is worse when he swallows.

On PE you note crepitus in the suprasternal notch and neck region + crunching sound on chest auscultation (Hamman). NO hematamesis.

You suspect

Answer 182

Boerhaave syndrome

What: Esophageal perforation (MC distally)
Due to: OH, Repetitive Vomiting (complication of esophageal….)

• crepitus: subcutaenous/mediastinal emphysema
• *NO hematemesis

Question 183

Esophageal: A patient who is a chronic alcoholic presents with repeated episodes of vomiting and severe retrosternal pain that radiates to the back.

On PE you note crepitus in the suprasternal notch (subcutaneous/mediastinal emphysema) and crunching sounds on chest auscultation (Hamman).

What is a potential complication of this syndrome?

a. pneumomediastinum
b. mediastinitis
c. sepsis and shock
d. death

Answer 183

All of the above

Boerhaave syndrome

• transmural perforation of esophageal wall, distal 1/3 (left dorsolateral)
• high mortality with esophageal rupture

Question 184

Esophageal: A crunching, rasping sound that is synchronous with a person’t heart beat. It is heard over the precordium.

Answer 184

Hamman’s sign

• due to the heart beating against air filled tissue (mediastinal air)
• *Boerhaave syndrome -pneumomediastinum

Question 185

Esophageal: Bening neoplasms of the esophagus include

1. ______: tumor of SM
2. Lipma: tumor of fat

Answer 185

Leiomyoma

Question 186

Esophageal: Malignant neoplasms include

1. Adenocarcinoma
2. Squamous cell carcinoma

____ occurs most often in black males. It is usually the proximal 2/3 of the esophagus. It is often associated with smoking and alcohol (synergistic effect)

Answer 186

Squamous Cell carcinoma

• high mortality
• progressive dysphagia
• weight loss (late)
• early lymph node metastasis

Question 187

Esophageal: Malignant neoplasms include

1. Adenocarcinoma
2. Squamous cell carcinoma

_____ is the MC 1o esophageal cancer in U.S. It most often affects white males (>60 y.o) and is common in the distal 1/3 of the esophagus. It is often associated with Barrett’s esophagus, which induces intestinal metaplasia.

Answer 187

Adenocarcinoma

• high mortality
• progressive dysphagia
• weight loss (late)
• early lymph node metastasis

Question 188

Esophageal: True/False - lack of serosa and extensive lymphatics allows esophageal cancer to spread early in the disease course

Answer 188

True

Question 189

Esophageal: Because it arises in Barrett’s mucosa, adenocarcinoma occurs in the distal esophagus. Which of the following accurately describes the progression to cancer?

a. gastroesophageal reflux – metaplasia – low grade dysplasia – high grade dysplasia – adenocarcinoma
b. gastroesophageal reflux – low grade dysplasia – metaplasia – high grade dysplasia – adenocarcinoma

Answer 189

A

–reflux – meta – low grade – high grade – carcinoma

Question 190

Esophageal: Contrast risk factors for adenocarcinoma and squamous cell carcinoma

Answer 190

Adenocarcinoma:
–smoking

Squamous cell:

• -smoking, alcohol
• -diet w/ few fruits/veg.
• -caustic ingestion
• -achalasia

Question 191

Esophageal: True/False - Squamous cell carcinoma often occurs in the mid-esophageus causing strictures. It most commonly occurs in black males

Answer 191

True

Question 192

Histo: THe major salivary glands are the parotid, submandibular and sublingual.

1. The ____ gland (serous) empties into the oral cavity opposite the 2nd upper molar. Secretion is stimulated by PNS (CN 9)
2. The ___ gland (mixed; mostly serous) empties into the oral cavity lateral to the frenulum of the tongue. Innervation is CN7 (facial; PNS).
3. The ___ gland (mixed; mostly mucous) empties into the submandibular duct and directly onto the floor of the oral cavity. Innervation is CN7 (facial; PNS)

Answer 192

1. parotid
2. submandibular
3. sublingual

Question 193

Histo:

1. Parasympathetic stimulation (Ach) stimulates secretion of what acinar cells?
2. Sympathetic stimulation (NE) stimulates secretion of what acinar cells?
3. _______ cells propel the product toward the excretory duct

Answer 193

1. Serous
2. Mucous

*myoepithelial cells = propel product toward excretory duct (actin filaments)

Question 194

Histo:

1. _____ ducts have low, cuboidal cells. They secrete HCO3- and absorb Cl-
2. _____ ducts have cuboidal to columnar cells. They reabsorb Na and secrete K+/HCO3-. *hypotonic secretion

Answer 194

1. Intercalated

2. Striated

Question 195

Histo: The function of the mucosa is to protect, secrete (mucous, digestive enzymes) and absorb). It consists of 3 layers:

1. Epithelium (changes depending on function)
2. Lamina propria (CT; glands)
3. Muscularis mucosa (SM)

What are the layers of the muscularis mucosa? What is its function?

Answer 195

2 layers: circular and longitudinal

fxn: localize movement of mucosa; absorption and secretion

Question 196

Histo: The submucosa lies below the muscularis mucosa. It is a layer of dense irregular CT with blood vessels and lymphatics. It also contains nerve plexi (ganglions whose nerve cell body is outside of the CNS). Describe signalling of these plexi

Answer 196

*Meissner’s

1. Visceral sympathetic sneosry
2. PNS terminal ganglia
3. Enteric (pre and post-PNS)

Question 197

Histo: The muscularis externa is composed of 2 layers of SM (inner circular and outer long.). Enlargements of this layer forms sphincters, and it contraction of the circular muscle helps mix contents of the lumen.

It also contains blood, lymph vessels and nerves. Describe the signalling

Answer 197

Myenteric plexus (Auerbach)

1. ganglions of post-ganglionic PNS
2. enteric

NOTE: circular: compress/mixing; long. muscle shortens tube and propels contents

Question 198

Histo: True/False - Enlargement of the inner circular muscle forms the sphincters and valves. These sphincters include:

1. pharyngoesophageal (UES)
2. Inferior (LES))
3. pyloric
4. ileocecal
5. internal anal sphincter

Answer 198

True

Question 199

Histo: The adventitia/serosa is the outermost layer of the gut. It is composed of dense, irregular CT.

1. _______ is found on organs that are suspended. It is simple squamous (mesothelial) and is equivalent to visceral peritoneum.
2. _____ covers regions of the tract not lined by serosa. It is found on organs that are attached to the body wall.

Answer 199

1. Serosa

2. Adventitia

Question 200

Histo: As the gut progresses caudally, we see a widened lumen, increased surface area, increased invaginations and evaginations (pits, crypts, villi) and which of the following?

a. goblet cells
b. basophilia
c. lymphoid tissue

Answer 200

all of the above

Question 201

Histo: The esophagus is a fixed muscular tube connecting the pharynx and stomach. It starts at the level of the cricoid cartilage and descends post. to the trachea.

The UES is striated (sk muscle) and functions to what?

Answer 201

block movement of air into the esophagus

NOTE:

• thoracic esophagus: adventitia;
• part of abdominal esophagus: serosa

Question 202

Histo: Describe the transition (histologically) from the esophagus to the stomach

Answer 202

Strat. squamous wet to simple columnar w/ pits and glands (invagination)

Question 203

Histo: The gastric epithelium contains surface mucous cells. It also invaginates forming gastric pits (openings) and gastric glands (bottom of pits).

What do the glands secrete?

Answer 203

Mucous (appear cloudy)

• protection
• HCO3-

Question 204

Histo: The following are cells of the fundic stomach. List their functions

1. Surface mucous cells (line surface and gastric pits; simple columnar)
2. Neck mucous cells (line neck; cuboidal)
3. Chief cells
4. Parietal cells
5. Enteroendocrine cells

*Pyloric stomach = loss of parietal and chief (mucous only)

Answer 204

1. Neck mucous
   - -alkaline mucous
   - -vagal stimulation
2. Parietal cells
   - -apex directed toward lumen
   - -HCL (protein digestion; converts pepsinogen to pepsin)
   - -IF (binds B12 — absorption)
3. Chief cells
   - -base of fundic glands (near muscularis mucosa)
   - -basophilic
   - -pepsinogen (activated pH < 5)
   - -bactericide

Question 205

PUD drugs: True/False - Mix of AlOH/MgOH antacids with or without simethicone can relieve symptoms of extra gas with fewer adverse effects (less diarrhea and constipation) than the respective Mg and Al only preparations

Answer 205

True

Question 206

Histo: List the cells of the Small Intestines and their secretions

1. Enterocytes
2. Enteroendocrine cells
3. Goblet cells
4. Paneth cells

Answer 206

1. Enterocytes
   - -
2. Enteroendocrine cells
3. Goblet cells
   - -
4. Paneth cells
   - -antibacterial (phagocytose gram - bacteria)
   - -lysozyme (degrades bacterial cell wall; form pores in plasma membrane)

Question 207

Histo: The transition from the esophagus to the stomach involves a change in epithelium. Describe the transition

Answer 207

Esophagus: stratified sq. wet
Stomach: simple columnar with pits and glands
–invagination

Question 208

Histo: Paneth cells are located at the base of the glands of the small intestines. Describe their features and their secretions.

Answer 208

Features:

• -basophilic cytoplasm
• -acidphilic, apical secretory granules

Secrete:

• -lysozyme
• -defensins (anti-microbial)
• -phospholipase A2
• -TNF-Alpha

Question 209

Histo: Enteroendocrine cells are found in both the stomach and the SI. They resemble neurosecretory cells of the CNS. They secrete basally, rather than into the lumen.

What are their secretions?

Answer 209

1. somatostatin (inhibit gastrin)
2. gastrin (inc. HCl)
3. ghrelin (inc. GH; appetite; inhibits lipid metabolism and fat utilization)
4. CCK – gallbaldder contraction; pancreatic enzyme secretion
5. GIP – inc. insulin; dec. gastric acid
6. VIP – inc. heart contractility; vasodilation
7. motilin – inc. motility

Question 210

Histology: HCl production is stimulated by gastrin (major path for stimulation), Histamine (H2 receptor) and Ach. Formation of HCl involves the movement of K+ into the cell — to the canaliculus lumen, back into the cell and out of the cell.

What are the steps in HCl production?

Answer 210

1. Formation of carbonic acid
   - -CO2 enters cell – H2CO3 – H+ + HCO3
2. Cl- enters the cell (exchanged for HCO3)
   - -anion exchange (basal surface)
   - -Cl- enters canaliculus
   - HCO3- enters capillaries (lamina propria) and mucus lining
3. Exchange K+ for H+
   - -via H+/K+ ATPAse
   - -H+ out of cell to lumen (canaliculus)
4. HCl formation
   - -in canaliculus

Question 211

Histo: What is the distinguishing feature of the pyloroduodenal junction?

Answer 211

Goblet cells scattered in gastric glands

Question 212

Histo: The small intestine acts as the principal site of digestion and absorption. It is composed of the duodenum, jejunum and the ileum.

The duodenum wraps around the head of the pancreas. Bile and pancreatic enzymes enter the ______ of the descending duodenum.

Answer 212

posteromedial wall

NOTE: duodenum is retroperitoneal (serosa - anterior; adventitia - posterior)

Question 213

Histo: Transverse, circular folds with a core of submucosa. They are found in the small intestine (primarily the duodenum) and aid in nutrient absorption.

*also known as finger-like projections with villi

Answer 213

Plicae circulares (valves of Kerckring)

• extend 1/2 to 1/3 around the circumference of the lumen
• most numerous in distal duodenum

NOTE: *villi contain lamina propria core and lacteals (blind ended lymphatic vessels)

Question 214

Histo: Intestinal glands (crypts of Lieberkuhn) of the small intestine span the width of the lamina propria. They open onto the luminal surface at the base of the villi. They contain several different cells including:

1. Enterocytes
2. Goblet Cells
3. Paneth Cells
4. Enteroendocrine cells

_______ are small, columnar cells with microvilli that function mainly in absorption. They are joined to neighboring cells by tight junctions and act to move water across the cell.

Answer 214

Enterocytes

a. Water movement: via lateral Na/K+ ATPase
- -intercellular bridges (Na moves in apically; out laterally)
- -water follows

b. enzymes localized to apical membrane (microvilli)
- -enteriokinase (trypsinogen to trypsin)
- -trypsin cleaves/activates other enzymes

Question 215

Histo: Intestinal glands (crypts of Lieberkuhn) of the small intestine span the width of the lamina propria. They open onto the luminal surface at the base of the villi. They contain several different cells including:

1. Enterocytes
2. Goblet Cells
3. Paneth Cells
4. Enteroendocrine cells

Enteroendocrine cells secrete hormones basally into the bloodstream (similar to those in the stomach, while Goblet cells (unicellular glands) contain large mucinogen granules apical to the nucleus. What do they secrete?

Answer 215

Mucin

(gets hydrated – protective gel coat – protects epithelial lining from abrasion and inhibits bacterial invasion

Question 216

Histo: Histo: Intestinal glands (crypts of Lieberkuhn) of the small intestine span the width of the lamina propria. They open onto the luminal surface at the base of the villi. They contain several different cells including:

1. Enterocytes
2. Goblet Cells
3. Paneth Cells
4. Enteroendocrine cells

Paneth cells are unique to the glands of the small intestine (though can appear in large intestine for pathologies). They are found at the base of the intestinal gland and secrete apically into the lumen. What do they secrete?

Answer 216

1. TNF alpha
2. Lysozyme: degrades bacterial cell wall and forms pores in plasma membrane
3. Defensins: + charge aa’s and hydrophobic aa’s to insert into membrane – pore – kills
4. Receptors (on plasma membrane): endocytosis of macromolecules and gram - bacteria

• *antimicrobial cells
• acidophilic/eosinophilic granules

Question 217

Histo: Histo: Intestinal glands (crypts of Lieberkuhn) of the small intestine span the width of the lamina propria. They open onto the luminal surface at the base of the villi.

They contain several different cells including Microfold (M) cells. M cells are located over lymphatic nodules (especially Peyer’s patches of the Ileum). They lack microvilli, but have apical membrane infoldings.

What is the function of M cells?

Answer 217

Transcytose antigens to underlying CT – deliver antigen to APC’s

Question 218

Histo: What is a distingyishing feature of the duodenum?

Answer 218

Brunner’s glands

• -secrete alkaline (pH 8.8-9.3) mucous and HCO3-
• neutralizes acidic chyme (stomach)
• -provides correct pH for activation of digestive enzymes from the pancreas

Question 219

Histo: The ileum and the jejunum have no submucosal glands. The jejunum has some lymphatic nodules, while the Ileum contains lymphatic nodules in the form of

Answer 219

Peyer’s patches

Question 220

Small Intestine disorders: The function of the small intestine is to increase the surface area for absorption. It is composed of the following:

1. Duodenum (Fe absorption)
2. Jejunum (Folate absorption)
3. Terminal ileum (B12 absorption)

Which part of the small intestine do you suspect to be affected in a patient with Down Syndrome (Trisomy 21) who presents with polyhydramnios, bilious vomiting, delayed passage of meconium and “double bubble” sign on radiograph?

Answer 220

Duodenal Atresia

• failure of canalization of the small bowel (a.k.a. complete occlusion or absence of a duodenal lumen)
• complete obstruction
• no gas distally, foaming at the mouth
• non-bilious vomiting if proximal to major duodenal papilla

NOTE: triple bubble sign = jejunal atresia (apple peel)

Question 221

Small intestine disorders: ___ refers to incomplete obstruction of the small bowel that is caused by narrowing of the segment. It is less common than atresia

Answer 221

Stenosis

Question 222

Small intestine disorders: ____ is characterized by persistence of the Vitelline (omphalomesenteric) duct. It follows the rule of 2’s:

1. ~2 inches long
2. 2 feet proximal to ileocecal valve
3. 2 % of the population
4. < 2 years old

Often presents asymptomatic, OR with painless hematochezia (lower GI bleed) with no signs of abnormalities on workup. It is considered a TRUE diverticulum.

Answer 222

Meckel’s diverticulum

*MC congenital malformation of the GI tract
*May contain heterotropic mucosa
(gastric MC – inc. risk of hemorrhage 2ndary to gastric acid)

NOTE: may present with RLQ pain; tarry stool

Question 223

Small intestine disorders: A 15 month old female presents with grossly bloody diarrhea for 2 days. She has had a few episodes of blood tinged stools over the past 2 weeks. Her mother denies pain, nausea or vomiting. You note conjunctival pallor. Abdomen is soft and nontender. A small amount of dark red blood is present in her diaper.

You suspect

Answer 223

Meckel diverticulum

*Bleeding associated with heterotopic gastric mucose (inc. gastric acid = ulcers); Inc. risk Fe deficiency

NOTE: incomplete obliteration of omphalomesenteric duct.

Classic symptoms: Painless lower GI bleeding (hematochezia) in kids < 2 years; labs usually normal

Question 224

Small Intestine disorders: A complication of Meckel’s diverticulum is intestinal obstruction. It can occur via attachment of the intestine to the abdominal wall by a fibrous band. A portion of the small bowel can then get wrapped around the band leading to volvulus. What can this lead to?

Answer 224

intussuception

Question 225

Small Intestine disorders: A 2 year old male is brought to the clinic for dark stools. His parents report 2 days of black, jelly like stool in his diaper. He has not been irritable or shown any signs of distress or pain.

The abdomen is soft and nontender with normal bowel sounds. You suspect Meckel’s diverticulum. How do you diagnose Meckel’s diverticulum?

Answer 225

Laparoscopy/Laparotomy

*Technetium scan (injected IV – accumulation in the gastric mucosa over time)

Question 226

Small Intestine disorders: There are different causes of bowel obstruction including:

1. herniation
2. adhesions
3. volvulus
4. intussusception (intestine telescopes into itself)

What are radiographic findings indicative of bowel obstruction?

Answer 226

• bowel distension
• air/fluid levels with step ladder appearance
• -absence of air distal to obstruction

Question 227

Small intestine disorders: What are signs/symptoms of bowel obstruction?

a. abdominal pain
b. bilious vomiting
c. constipation
d. no rebound tenderness (no peritonitis)

Answer 227

all of the above

• abdominal distension
• *non-bilious emesis if PROXIMAL to ampulla of Vater

Question 228

Small Intestine Disorders: A patient presents with colicky abdominal pain, constipation and vomiting. You note abdominal distension.

PMH Abdominal Surgery

You suspect the development of

Answer 228

Adhesions

• fibrous bands between loops of bowel.
• MCC small bowel obstruction
• secondary to peritoneal inflammation (previous surgery)

Question 229

Small Intestine disorders: A protrusion, bulge or projection of an organ or a part of an organ through the body wall that normally contains said organ.

Clinically you see:

1. swelling or fullness at site
2. heavy, aching sensation (radiates to area)
3. no true pain or tenderness on PE
4. enlarges w/ increasing pressure (cough, lifting)

Answer 229

Hernia

Question 230

Small Intestine disorders: Distinguish between an indirect and a direct hernia. How do these differ from a femoral hernia?

Answer 230

1. Indirect
   - -strikes distal tip of finger
   - -superolateral to inferomedial
   - Indirect Lateral to Inferior Epigastric
   - processus vaginalis
2. Direct
   - -strikes pad of finger (deep to superficial)
   - Medial to Inferior Epigastric
   - weakened transvers fascialis?
   - regresses when reclined
3. Femoral hernia
   - -bulge felt below inguinal ligament

Question 231

Small Intestine disorders: Indirect inguinal hernias can form as a result of increased intra-abdominal pressure (e.g. coughing, lifting heavy weights) or from abdominal wall weakness.

It is MC associated with obesity, the male gender, and weight lifting. How does it differ in pathogenesis b/t adults and kids?

Answer 231

1. Kids
   –peritoneal connection persists
   (inguinal canal and tunica vaginalis)
2. Adults
   - -weak peritoneum
   - -small bowel passes through internal inguinal ring —through ext. inguinal ring – scrotal sac

Question 232

Small Intestine disorders: The triangle of Hesselbach is composed of:

1. Medial: rectus abdominis
2. Lateral: Inf. epigastric artery
3. Inferior: Inguinal (puopart’s ligament)

Indirect Inguinal Hernias occur outside of Hesselbach’s triangle. They ENTER the inguinal canal lateral to the ______ and EXIT the inguinal canal inferior to the ______.

Answer 232

1. ENTER - lateral to inf. epigastric

2. EXIT - inferior to inguinal lig.

Question 233

Small Intestine disorders: The triangle of Hesselbach is composed of:

1. Medial: rectus abdominis
2. Lateral: Inf. epigastric artery
3. Inferior: Inguinal (puopart’s ligament)

Direct Inguinal Hernias occur within Hesselbach’s triangle. They tend to breach the posterior inguinal wall and pass medial to the _________ vessels.

Answer 233

pass medial to inf. epigastric vessels

Clinical:

• -bulges in proximity to ext. inguinal ring
• disappears when patient reclines
• rarely incarcerates

Question 234

Small intestine disorders: A 31 year old female presents with peritoneal outpouching that extends into the femoral canal (medial to the femoral vein).

On PE you note absent scrotum involvement. It is not felt by the finger in the inguinal canal.

You suspect

Answer 234

Femoral hernia

• MC females
• highest rate of incarceration of the small bowel
• due to: narrow femoral ring

NOTE:

• never involves scrotum
• not felt by finger in inguinal canal

Question 235

Small intestine disorders: _____ in children occurs from an opening in the linea alba, which develops when the umbilical scar fails to heal at birth. It is MC in African American children. Most will close in the 1st 12-13 mos of life.

Answer 235

Umbiical hernia

kids: opening in linea alba
adults: acquired; inc. intra-ab pressure (pregnancy, obesity); MC females

Question 236

Small Intestine disorders: _____ describes a hernia in the area of previous surgical incision (a.k.a. incisional hernia).

Risk factors include anything that inhibits natural wound healing (e.g. infection, excessive wound tension, poor technique and obesity)

Answer 236

Ventral hernia

*obesity - creates tension on abdominal muscles

Question 237

Small Intestine disorders: ____ describes loops of bowel caught between adhesions that result in compromise of blood supply and subsequent infarction.

Answer 237

Internal hernia

Question 238

Small intestine disorders: complications of hernias include incarceration and strangulation.

1. ______ is due to compromise of blood flow to the herniated bowel. (leads to hemorrhagic infarction/ischemic bowel).
2. _____ is a hernia that cannot be reduced (spont. or mannually) thorugh the defect in the fascia. Associated with nausea, vomiting, bowl obstruction symptoms.

Answer 238

1. Strangulation

2. Incarceration

Question 239

Small Intestine: _______ occurs in elderly females. It is due to inflamed gallbladder that adheres to the small bowel and develops a fistula.

It can present with intermittent small bowel obstruction, presence of gallstones in the iliac fossa, and pneumobilia (gas in biliary tract).

Answer 239

Gallstone ileus

*gallstones pass through fistula

Question 240

Small intestine: ________ occurs when a segment of bowel becomes twisted on itself. It occurs in areas with redundant mesentery (small bowel, sigmoid or cecum).

Patients present with abdominal pain, distension, bilious vomiting or ischemia (gnagrene, tachycardia, hypotension and hematochezia).

Labs reveal:

1. Whirl sign or coffee bean sign and dilated loop of bowel (adults)
2. Cork-screw duodenum kids
3. Malpositioned duodenojejunal junction

Answer 240

Volvulus

• restricts blood supply – abdominal pain (infarction)
• bowel obstruction - bilious emesis
• Sigmoid MC adults, Midgut and Malrotation MC kids

Question 241

Small intestine: _______ is a proximal segment of bowel (intussusceptum) that invaginates into the distal segment (intussusipiens). Peristalsis tends to pull the mesentery with it.

Answer 241

Intussusception

complications: obstruction and infarction
due to: Meckel, peutz-jegher, Peyer’s patches

Question 242

Small intestine: What is believed to be the nidus for intususception in kids (MC < 5 y/o)?

a. polyp
b. cancer
c. lymphoid hyperplasia of Peyer’s patch
d. weight lifting

Answer 242

C - lymphoid hyperplasia of Peyer’s patch

*2ndary to viral infection (rotavirus vaccine)

Adults:
–polyp or cancer

Question 243

Small Intestine: A 4 year old child presents to the clinic with his concerned mother. She states that her son has been vomiting, and has been “colicky” with severe and intermittent abdominal pain. She confirms that he has had dark red, gelatinous “currant jelly” stools. She reports the “attacks” have been occurring every 15-30 minutes.

You note emptiness/retraction in the RLQ “Dance sign” on PE.

You suspect

Answer 243

Intussusception

*MCC Meckel diverticulum, Enlarged Peyer’s patches (rotavirus, adenorus, IgA vasculitis), Puetz Jegher

Clinical Triad: abdominal pain, palpable sausage-shaped mass and “currant jelly stools” (mucous + sloughed mucosa + shed blood)

Dx: Ultrasound

Question 244

Intestinal disorders: Disaccharide enzymes are located in the brush border of the SI villi. These enzymes aid in digestion of disaccharides into sugars.

Lactase deficiency (disaccharidase deficiency) is a malabsorption syndrome characterized by inability to digest lactose. This results in abdominal pain, flatus, and osmotic diarrhea upon ingestion of dairy products. Distinguish b/t primary and secondary deficiencies.

Answer 244

Primary:

• -genetic loss of lactase
• -MC non-white

Secondary:

• -viral infections of SI (damage villi – self-limited deficiency)
• -celiac disease

Question 245

Intestinal disorders: Pancreatic insufficiency occurs when > 90% of pancreatic exocrine function is lost. Loss of pancreatic enzymes (amylase and lipase) can lead to fat malabsorption.

What are clinical features of pancreatic insufficiency? What are common etiologies?

Answer 245

Clinical:

• -steatorrhea (loose, greasy, fould smelling stools)
• -deficiencies of fat-soluble vit. (ADEK)
• -loss of proteases (protein malabsorption)

Etiologies: CF, Chronic pancreatitis, Pancreatic duct obstruction (cancer)

Question 246

Intestinal disorders: ________ (sprue; gluten sensitive enteropathy) is due to an autoimmune reaction triggered by environmental agent (gliadin component of gluten) in genetically pre-disposed individuals.

It is common and is associated with IgA antibodies to gliadin, endomysium and tissue transglutaminase.

Answer 246

Celiac disease

• IgA to gliadin, endomysium, tissue transglutaminase
• HLA-DQ2 and/or HLA-DQ8 +

Question 247

Intestinal disorders: In genetically susceptible individuals with celiac disease, ingestion of food containing gluten (wheat, barley, or rye) induces an immune reaction.

deamidated Gliadin and tissue transglutaminases are presented to helper T-cells by APC’s. These T-helper cells mediate inflammation by releasing IFN and triggering B-cells to make autoantibodies.

What is the net result?

Answer 247

-destroyed villi – dec. surface area – malabsorption

1. gliadin presented to HLA DQ2 or HLA DQ8 on APC
2. Stimulate CD 8 T-cells (IL-15)
3. B cells and cytokines = tissue production

Question 248

Intestinal disorders: Patients with celiac disease typically present with manifestations due to malabsorption, including:

• nutritional deficiencies (B12, iron, folate, Ca2+)
• weight loss
• diarrhea
• flatulence
• weakness/fatigue (2ndary to nutritional deficiency/anemia
• -osteoporosis

What are histological features of celiac?

Answer 248

1. Loss of villi (villous atrophy) crypt hyperplasia
2. increase intra-epithelial T-cells

*villi may be flattened (less surface area for absorption)

Question 249

Small intestine disorders: Which of the following is an association of celiac disease?

a. dermatitis herpetiformis
b. Down syndrome
c. selective IgA deficiency
d. autoimmune disorders (type 1 diabetes mellitus, thyroiditis)

Answer 249

all of the above

1. derm. herpetiformis
   - -autoimmune
   - -blisters

Question 250

Small intestine disorders: _______ is associated with celiac disease. It is an autoimmune blistering disorder that results from an immunologic response to chronic stimulation of the gut mucosa by dietary gluten.

It presents as grouped vesicles (analagous to herpes; “herpetiformis”).

Answer 250

Dermatitis herpetiformis

*IF - IgA autoabs at tips of dermal papillae

Question 251

Small intestine disorders: Which of the following is true about celiac disease?

a. increased incidence in 1st degree relatives
b. high incidence in whites, low in blacks and asians
c. increased risk for adenocarcinoma and lymphoma
d. may have antibody testing or biopsy for confirmation
e. histology reverts to normal if started on gluten-free diet

Answer 251

All of the above

Dx:

1. Ab testing
   - -IgA anti-tissue transglutaminase ab (IgA tTG) **screen
   - -anti-endomysial ab
2. Biopsy
   - -confirm
   - -distal duodenum/proximal jejunum (**highest conc. of gluten)
   * crypt hyperplasia, villous atrophy

Question 252

Small intesting disorders: True/False - All patients express the HLA-DQ2 or HLA-DQ8 allele, however, only minority of people who express DQ2/DQ8 have celiac disease. Absence of these alleles excludes the diagnosis of celiac disease

Answer 252

True

Question 253

Small intestine disorders: Treatment for celiac disease includes starting the patient on a gluten-free diet and correcting the nutritional deficiencies.

If a patient who was previously doing well on gluten restriction is no longer responsive to the gluten restriction, what must be considered?

Answer 253

malignancy

*small intestinal lymphoma

Question 254

Histo: The large intestine joins the small intestine at the ileocecal junction. It functions to resorp H2O and electrolytes as well as eliminate waste. Two of the distinguishing features include taniae coli (colon and cecum) and NO villi (surface amplification).

What are other features of the large intestine?

a. absence of plicae circulares
b. absence of paneth cells in glands
c. absence of digestive enzymes
d. increased goblet cells
e. microfold cells

Answer 254

all of the above

4:1 enterocyte to goblet cell
(absorption, lubrication - mucous, NO digestion)

• muscularis externa w/ taenia coli (longitudinal muscle; 3 bands)
• haustra - localized sacs (contraction) of the taenia coli

Question 255

Histo: True/False - The outer longitudinal layer of muscularis externa of the large intestine is composed of taenia coli, 3 thickened, equally spaced bands of smooth muscle. Contraction of this smooth muscle forms haustra.

Taenia coli are NOT found in the rectum, anal canal or appendix.

Answer 255

True

• contractions of inner circular: segmentation (local)
• contractions of circular and longitudinal: peristalsis (distal mass movements)

Question 256

Histo:

1. ____ small blind pouch of large intestine that is histologically identical to the colon.
2. ____ slender, blind diverticulum of the cecum. It is small with an irregular lumen. It contains cellular debris.

Answer 256

1. Cecum
   - -ileocecal junction
2. Appendix
   - -uniform outer long. layer
   - -lots of lymphatic nodules (Peyer’s) in submucosa
   - -lymphocytes!

*intestinal glands, enterocytes, goblet cells

Question 257

Histo: The ______ is the dilated distal portion of the alimentary canal. It has transverse rectal folds that help to distinguish the upper region from the rest of the distal colon.

The mucosa of the rectum is similar to the distal colon with straight tubular glands and lots of goblet cells (1:1 enterocyte to goblet).

Answer 257

Rectum

Question 258

Histo: The anal canal is the most distal region of the alimentary canal. It is composed of longitudinal folds of mucosa in the upper region known as ____1___. It also contains depressions between these columns known as ___2___.

Mucus anal glands open into the anal sinuses. When compressed by fecal material, these sinuses exude mucous.

Answer 258

1. anal columns

2. anal sinuses

Question 259

Histo:

1. Zone of the anal canal that is composed of simple columnar with goblet cells
2. Zone of the anal canal that transitions from columnar – strat squamous wet epithelium.
3. Zone of the anal canal that is composed of stratified squamous dry epithelium

Answer 259

1. Colorectal zone (upper 1/3)
2. Anal transitional zone (pectinate line)
3. Squamous zone (lower 1/3)

• superior to pectinate line - derived from embryonic hindgut (endoderm)
• inferior to pectinate line - derived from embryonic proctodeum (ectoderm)

NOTE: above - superior rectal artery, portal system, internal iliac LNs

NOTE 2: Below - middle and inferior rectal, caval system, superficial inguinal, pudendal nerve (sensitive to pain)

Question 260

Histo: The submucosa of the large intestine contains thin-walled branches of the superior rectal artery and rectal venous plexusa.

Explain the clinical types of bleeding in association with the pectinate line

Answer 260

1. Superior to line:
   - -internal hemorrhoids
   - -intact musc. mucosa
2. Inferior to pectinate
   - -external hemorrhoids

Question 261

Histo: The internal anal sphincter is formed by the _____ layer of the muscularis externa of the large intestine

Answer 261

inner circular SM

• inner circu. thickens at the pectinate line
• SNS = inc. contraction
• PNS = inhibit contraction; inc. distension (movement of feces)

Question 262

Histo: The external anal sphincter is formed by _____ of the muscularis externa. It is under voluntary control and is the inferior 2/3 of the anal canal.

Answer 262

Skeletal muscle

*inf. to pectinate line

Question 263

Histo: The entire anal canal is embedded in surrounding CT (Adventitia). Blood supply and innervation is based upon association with pectinate line.

1. Describe blood supply/innervation superior to pectinate
2. Describe blood supply/innervation inferior to pectinate

Answer 263

1. Superior
   Nerve: visceral motor = stretch sensitive
   Lymph: internal iliac nodes
   Supply: IMA and exits hepatic portal
2. Inferior
   Nerve: somatic motor and sensory (parietal; pain, touch, temp)
   Lympy: superficial inguinal nodes
   Supply: Internal Iliac to IVC

NOTE: SNS: maintains tonus (contraction); PNS inhibits tonus

Question 264

Histo: True/False - Portal hypertension induces internal hemorrhoids

Answer 264

True

Question 265

Small intestine disorders: ______ is only found in certain (tropical areas of the world). Manifestations of this disorder are similar to those of celiac disease: chronic diarrhea, steatorrhea, weight loss and nutritional deficiencies.

Biopsy findings include:

1. villous damage/inflammation
2. NOT confined to proximal small bowel (unlike celiac)
3. damage to jejunum (folate deficiency)
4. damage to ileum (B12 deficiency)

It is thought to occur from infection (b/c it is responsive to antibiotics).

Answer 265

Tropical sprue

Dx:

• -abnormal SI biopsy in an individual with chronic diarrhea and evidence of malabsorption
• *reside in tropical country

Question 266

Small intestinal disorders: Growth of colonic type bacteria (E. coli, Bacteroides) within the small intestine.

It most often occurs from impaired peristalsis (scleroderma) or changes in intestinal anatomy (Crohn’s w/ fistula formation b/w small and large bowel)

Answer 266

Bacterial overgrowth

Clinical:

• -B12 def (bacteria use)
• -Steatorrhea (deconjugate bile acids – more quickly absorbed and not digestable)
• -diearrhea (due to steatorrhea and inc. fluid secretion from bacterial enterotoxins)

Question 267

Small intestine disorders: A rare, multi-system disorder with insidious onset of diarrhea, steatorrhea and weight loss.

It is MC due to SI involvement of Tropheryma whippelii, which causes malabsorption of fat. Lacteals get compressed by foamy macrophages containing the organisms.

Answer 267

Whipple disease

MC middle aged white men

*can involve other tissues (synovial tissues; arthralgia or CNS; dementia)

**Cardiac, Arthralgias, Neurologic, PAS (+) macrophages (foamy)

Question 268

SMall intestine disorders: Whipple disease can be ID’d based on the presence of bacteria, and the irregular fold patterns and thickened walls of the SI. Describe treatment and prognosis of whipple disease

Answer 268

Treatment:
–DS TMP-SMX 1x year

Prognosis: death within one year without treatment

Question 269

Small intestine disorders: Most of the SI is supplied by the SMA. Infarctions may occur leading to ischemia.

Types include:

1. ____: a full-thickness infarct that affects the entire wall. It is usudally due to embolism or thrombosis of the SMA.
2. ____: usually occurs 2o to hypoperfusion (shock)

Answer 269

1. transmural

2. superficial

Question 270

Small intestine disorders: Most of the SI is supplied by the SMA. Infarctions may occur leading to ischemia. Causes of acute ischemia include

1. Acute vascular obstruction
2. Non-occlusive ischemia
3. Mesenteric vein thrombosis

What are examples of each?

Answer 270

1. Acute vascular obstruction
   - embolism from heart (a-fib),
   - -aorta (atherosclerotic plaque), aortic aneurysm, SMA thrombosis
2. Non-occlusive ischemia
   - -shock
3. Mesenteric vein thrombosis
   - -hypercoagulable state, tumors

Question 271

Small intestine disorders: A patient presents with sudden onset severe abdominal pain and bloody diarrhea.

On PE you note absent bowel sounds (ileus) with NO rebound tenderness (peritonitis).

Labs reveal:

1. Profound neutrophilic leukocytosis
2. Positive stool guaiac
3. “thumbprint” sign on CT

What do you suspect?

Answer 271

Small bowel infarction

Dx: Abdominal CT **

• -“thumbprint sign” (edema in bowel wall)
• -bowel distension w/ air or fluid levels similar to obstruction

Question 272

Small intestine disorders: Diverticular disease is uncommon in the small bowel, but if it occurs, it is MC in the duodenum.

It is associated with systemic sclerosis, and can result in _____ due to bacterial overgrowth.

Answer 272

B12 deficiency

Question 273

Small intestine disorders: A 2 week old, low birth weight infant is brought into the ER due to bloody stool.

On PE you note abdominal distension and presence of gas in the intestinal wall (pneumatosis intestinalis).

You admit the patient and refer to surgery for resection because you suspect

Answer 273

Necrotizing enterocolitis

• ischemic necrosis of small/large intestine
• premature, low birth weight infants

COmplications:

• -transmural necrosis w/ perforation and peritonitis
• -strictures from healing

Treatment:
–resect damaged segment

Prognosis:
–high mortality

Question 274

Small intestine: The MC malignancy of the small bowel is metastatic disease. Primary malignant tumors of the small bowel include:

a. carcinoid tumor within the terminal ileum
b. adenocarcinoma in the duodenum or proximal jejunum
c. malignant lymphoma in the terminal ileum
d. duodenal carcinoma

Answer 274

A-C

1. Carcinoid:
   - -ileum or more proximal
   - -MC 1o malignancy of SI
2. Adenocarcinoma
   - -rare
   - -MC ampulla of Vater
   - -inc. risk with FAP
3. Malignant lymphoma
   - -B cell origin (extra-nodal marginal zone; MALT)
   - -T cell if secondary to celiac

Question 275

Small Intestine disorders: Tumor of neuroendocrine origins that can be potentially malignant (depends on presence of metastasis).

It is characterized by monotonous sheets and nests of small round cells with uniform nuclei and absent to rare mitotic figures.

Answer 275

Carcinoid tumor

• -immunohistochemical stain: chromogranin
• -more likely malignant wit inc. size (>2cm)

*small bowel carcinoids = more likely to metastasize than stomach/rectum

Question 276

Small intestine disorders: Carcinoid syndrome is possible when a carcinoid tumor has metastasized to the liver. Normally, serotonin (5HT) from the tumor travels to the liver through the portal circulation, where it is metabolized to 5-HIAA.

What occurs in the case of metastatic tumor nodules?

Answer 276

5HT is directly secreted into hepatic vein tributaries (systemic circulation)

Question 277

Small intestine disorders: A 41 year old female presents to the clinic with intermittent wheezing, episodic facial flushing, abdominal cramps and secretory (watery) diarrhea.

Past medical history includes cardiac valvular abnormalities (tricuspid insufficiency or pulmonary stenosis) and heart disease (mainly R. sided heart fibrosis).

Imaging reveals a mass in the small bowel (MC ileum). Histology reveals prominent rosettes composed of numerous small monomorphic cells with salt and pepper chromatin. Cells stain positive for synaptophysin, chromogranin A and neuron specific enolase (NSE).

What do you suspect?

Answer 277

Carcinoid tumor

–5HT (Inc. 5HIAA)

1. flushing of the skin (2ndary to vasodilation)
   - -warmth
   - -stress, OH, exercise, cheese
   - -5HT inc. bowel secretions/motility

NOTE: Neuroendocrine tumor (enterochromaffin cells of GI, B-cells of pancreas)

Question 278

Small intestine disorders: Carcinoid heart disease is a common complication of carcinoid syndrome. It is caused by fibrotic plaques of the R. sided heart valves (not L. sided because MAO in the lung metabolizes 5HT to inactive 5HIAA).

Carcinoid heart disease primarily results in what?

Answer 278

1. tricuspid regurg.
   - -high pitched, holosystolic murmur at left lower sternal border)
2. pulmonary stenosis

Question 279

Small intestine disorders: True/False - Adenomatous polyps that are dysplastic (pre-cancerous) can be a risk of transformation into adenocarcinoma

Answer 279

True

Question 280

Inflammatory Bowel: IBD encompasses Ulcerative colitis and Crohn disease.

Under physiologic conditions, homeostasis normally exists b/t the commensal microbiota, intestinal epithelial cells and the immune system. In the case of UC and Crohn, disruption of these relationships via genetic factors or environmental factors has occurred.

Answer 280

True

*disrupt homeostasis – inflammation (IBD)

Question 281

IBD: Inlammatory bowel disease affects a wide age rang, but peak incidence occurs in the 2nd to 4th decades. It affects males and females equally, but is most prominent in white urban populations (esp. Jewish).

Manifestations depend on the area of the tract involved, but MC include cramping, abdominal pain, diarrhea +/- passage of mucous or blood. What is unique about these symptoms?

Answer 281

Wax and wane in intensity

• symptomatic: active stage
• asymptomatic: Inactive stage

Question 282

IBD: Ulcerative colitis always involves the rectum (usually starting point) and progresses in a continuous fashion.

What are the major symptoms of ulcerative colitis?

a. rectal bleeding
b. tenesmus
c. passage of mucous
d. cramping/abdominal pain

Answer 282

All of the above

1. rectal bleeds
   - -fresh blood/blood stained mucous
   - -may be mixed with stool or streaked onto the surface of the stool
2. Tenesmus
   - -urgency with a feeling of incomplete evacuation

NOTE: severity of symptoms correlates with extent of disease. May present acutely, but MC chronic symptoms.

Question 283

IBD: On imaging, ________ can appear with erythematous finely granular inflamed mucosa. It may bleed depending on severity of inflammation.

Lead pipe sign (loss of haustra) also key finding

Answer 283

ulcerative colitis

Question 284

IBD:

1. Ulcerative colitis is limited to what structure?
2. Describe the inflammation
3. What is the cancer risk?

Answer 284

1. Limited to colon/rectum
   - -starts at anal verge (involves rectum)
   - -may remain confined there, or proximal contiguous extension
   * NO skip lesions
2. Superficial, NO granulomas
   - -ulceration = bleeding, fluid/electro loss
   - -activity waxes and wanes (trigger = psychological stress)
3. After 8-10 years, substantial inc. risk of colon cancer
   * colonoscopy and surveillance biopsy every few years

Question 285

IBD: True/False - With ulcerative colitis, intestinal manifestations are surgically curable. However, extra-intestinal manifestations persist.

Answer 285

True

*Perinuclear anti-neutrophil cyoplasmic antibody (pANCA) may be elevated

Question 286

IBD: Complications of Ulcerative colitis include

a. massive hemorrhage with severe attacks
b. toxic megacolon
c. perforation leading to peritonitis
d. strictures due to scarring
e. colon cancer

Answer 286

all of the above

1. massive hemorrhage
   - may require colectomy
2. megacolon - massive dilatation;
   - -half resolve with therapy
   - -if doesn’t resolve = urgent colectomy
3. perforation - associated with toxiic megacolon
   - -inc. mortality
4. Colon cancer
   - -esp. long standing (> 10 years) and extensive disease (>50% colon involvement)

Question 287

IBD: A patient presents complaining of abdominal pain and cramping. He states he has bloody stool.

Gross findings reveal “inflamed colonic mucosa with “pseudopolyps”

Labs reveal elevated P-ANCA

You suspect

Answer 287

Ulcerative colitis

• areas of regenerating mucosa projecting into the lumen
• continuous involvement - no skip areas

Question 288

Unlike UC, which only involves the colon/rectum, Crohn disease can onvolve any region of the GI tract (mouth to anus - MC terminal ileum and ascending colon).

The site of the disease influences the clinical presentation (more variable manifestations than in UC).. However, Crohn’s commonly presents with diarrhea and inflammation. Describe the inflammation compared to UC

Answer 288

full-thickness (transmural)

*inc. risk fibrosis (strictures, obstruction), fistulae and perianal obstruction

Question 289

IBD: Although Crohn’s can involve any region of the GI tract, the most common sites affected are

Answer 289

Terminal ileum +/- ascending colon

*iliocolitis: chronic Hx of recurrent R. lower quad pain and diarrhea (may mimic acute appendicitis)

Question 290

IBD: Crohn’s disease is most common in what populations?

Answer 290

Whites (eastern European) or Ashkenazi Jews

• 2 peaks of incidence: teens - 20s; 60-70
• slightly more common in males

Question 291

IBD: Which of the following does NOT describe Crohn’s disease?

a. Only involves the rectum
b. Skip lesions
c. transmural
d. granulomas are characteristic

Answer 291

A - only involves rectum

• any segment of GI (often spares rectum)
• perianal complications (pain, abscesses, drainage)
• skip lesions (periodic remissions/exacerbations; inflammation)

*granulomas (macrophages)

Question 292

IBD: Granulomas are characteristic of Crohn’s disease. They are not surgically curable, and recurrences are common.

How are they detected? What is their significance?

Answer 292

*inc. risk of colon cancer (less than UC)

detection:
–Anti-saccharomyces cerevisiae antibody (+
ASCA +)

Question 293

IBD: What are (characteristic) gross/lab findings of Crohn’s?

Answer 293

Gross:

1. cobblestoning (disease tissue below normal mucosa)
2. creeping fat (narrowed lumen – fat pulled with it around bowel wall)

Endoscopy:

• -stricture
• -“string sign”
• healing w/ fibrosis = thickened bowel wall w/ narrowed lumen

Histology:
–granulomatous inflammation (non-caseating/non-necrotic)

Question 294

IBD: True/False - True/False - The transmural nature of the inflammation in Crohn’s disease usually leads to Increased risk of obstruction and fistula formation. Obstruction occurs from decreased luminal diameter due to fibrosis, whereas fistulae formation occurs from ulcers extending into deeper tissue.

Answer 294

True

*segmental nature results in gaps of normal or dilated bowel b/t involved segments

Question 295

IBD: Common complications of Crohn’s disease are malabsorption of bile salts and vitamin B12.

Bile salts are normally absorbed in the distal ileu. Depletion of the bile salt pool can lead to risk of fat malabsorption and ultimately the development of ____

Answer 295

steatorrhea

• contributes to other issues:
• -malnutrition, weight loss
• -hypocalcemia, clotting, osteomalacia
• -pigment gallstones (reduced bile acid:cholesterol ratio = lithogenic bile)

Question 296

IBD: Toxic megacolon is due to acute, severe colitis with markedly dilated colon (non-obstructive colonic dilatation >6cm).

It is a medical emergency, and has a high risk of perforation (lethal). It is most commonly associated (but not specific to) which bowel disorder?

Answer 296

Ulcerative colitis

Question 297

IBD: True/False - Both IBD syndromes can occur with extra-intestinal manifestations. Arthritis is more common in patients suffering from Crohn’s disease, whereas primary sclerosing cholangitis is most often seen in ulcerative colitis patients.

Answer 297

True

Question 298

Gastric disorders: Protective factors of the stomach include:

1. mucin (secreted by surface foveolar cells) which forms a barrierr
2. HCO3- (neutralizes pH)
3. Gastric epithelial cells (replaced every few days; form barrier and limit back diffusion)
4. Blood lfow (O2, nutrients and washes away back-diffused acid)

Prostaglandins also play a major role in protection of the stomach. They do so by regulating what?

Answer 298

HCO3- secretion, mucosal blood flow and epithelial regeneration

NOTE: NSAIDs act by inhibiting COX-1 – dec. prostaglandins – degrade protective ability of stomach

Question 299

Gastric disorders:

1. ____ describes vomiting of blood. The MC causes are Gastric and/or duodenal ulcers (PUD). Gastritis, esophagitis, Mallory Weiss can also contribute.
2. ____: black tarry stool. Presence indicates an upper GI bleed

Answer 299

1. Hematemesis
2. Melena
   - -proximal to duodeno-jejunal jxn (ligament of Treitz)
   - -Hb converted to hematin (black pigment) by acid

Question 300

Gastric disorders: Gastric acid can be analyzed using Basal acid output (BAO) and Maximal acid output (MAO). BAO is output of gastric fluid that is collected via NG tube over a 1 hour period on an empty stomach, whereas, MAO describes fluid collected over 1hr following pentagastrin administration.

What would you expect these values to look like in a patient with gastric ulcers? duodenal ulcers?

Answer 300

1. Gastric
   - -normal or decreased BAO, MAO
2. Duodenal
   - -increased BAO and MAO

Question 301

Gastric disorders: Progressive hypertrophy of the circular muscles of the pyloric sphincter is characteristic of ________. It is not present at birth, but occurs over the ensuing 3-5 weeks. It is believed to be due to genetic dysfunction.

Clinical presentation includes:

1. non-bilious, projectile vomiting
2. palapable “olive” abdominal mass (thickened pylorus)
3. visible hyperperistalsis

Answer 301

Infantile Hypertrophic Pyloric stenosis

• MC males and siblings
• hungry eater

Dx: Abdominal ultrasound
Tx: pyloromyotomy – split muscle layer to relieve obstruction

NOTE: stenosis can be acquired secondary to scarring from PUD

Question 302

Gastric disorders: Delayed gastric emptying of food that results in early satiety, nausea and vomiting of undigested food after eating.

It is commonly idiopathic, but may be due to autonomic neuropathy, post-vagotomy, or Ach medications.

Answer 302

Gastroparesis

Question 303

Gastric disorders: Damage to the gastric mucosa with erosion and subsequent hemorrhage.

It is caused by direct toxicity and/or mucosal ischemia that leads to mucosal injury enabling entry of gastric acid or pepsin to penetrate the mucosa.

Answer 303

Acute hemorrhagic erosive gastropathy

• acid penetrates mucosa
• MC alcoholics (direct toxic effect)

Other etiologic agents: cancer chemo; caustic ingestions (acid or alkali); iron pills (mucosal necrosis, erosions, ulcers); cocaine (vasoconstriction of mesenteric vasculature - ischemia)

Question 304

Gastric disorders: Stress ulcers are associated with severe physiologic stress (e.g. trauma, burns, major surgery).

There are two main Pathogenesis:

1. Ischemia secondary to decreased mucosal blood flow
2. Increased vagal stimulation

Explain

Answer 304

1. Ischemic injury
   - -systemic hypoperfusion (shock)
   - -hypovolemia due to severe burns (Curlings ulcer)
2. Vagal stimulation
   –CNS injury or disease (inc. intra-cranial pressure) – inc. vagal outflow – parietal cell activity – inc. acid
   (Cushing’s ulcer)

Question 305

Gastric disorders: Peptic ulcer disease (PUD) describes a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall.

Many present without symptoms, or present following the onset of complications (hemorrhage or perforation). Some present with upper abdominal (epigastric pain).

What are common etiologies of ulcers? What is MCC?

Answer 305

1. H. pylori ***
   - -declining prevalence of infection
   - -eradication reduces recurrence
   * smoking
2. NSAIDS
3. Severe stress (life-threatening illness)
4. Excess gastric acid (Zollinger Ellison)

NOTE: duodenal ulcers MC than gastric; avoid smoking and OH

Question 306

Gastric disorders: A 41 year old patient presents complaining of burning “gnawing” epigastric pain. He states it improves when he eats, but is worse about 2-5 hours after meals. He also complains the pain is worse at night. The previous describes what type of ulcer?

Answer 306

Duodenal

• Worse – when acid is secreted in absence of food to buffer
• worse at night - max circadian acid secretion

Question 307

Gastric disorders: A 36 year old female presents to the clinic complaining of epigastric pain that worsens when she eats. She complains of weight loss and nausea. This describes what type of ulcer?

Answer 307

Gastric ulcer

Question 308

Gastric disorders: The following gross and microscopic findings describe what disorder?

Gross: Well circumscribed with slight elevation around the edges “punched out lesions”

Microscopic:

• necrotic debris with neutrophils
• heals with scarring (fibrosis)

Answer 308

Peptic ulcer disease

Scarring = inc. risk gastric outlet obstruction

NOTE:

• Gastric ulcers = Biopsy ** (due to risk of ulcer being caused by gastric cancer)
• Duodenal ulcers = no biopsy needed; not malignant

Question 309

Gastric disorders: Complications of PUD include:

1. Hemorrhage (MC)
2. Perforation
3. Gastric outlet obstruction

____ is the MC complication. It may be significant/lethal. Increased risk is in older adults. It presents with melena, hematamesis and “coffee ground” emesis.

Answer 309

Hemorrhage

• coffee grounds
• Inc. BUN (absorption of proteins; pre-renal azotemia)

NOTE: gastric bleeds - left gastric artery; duodenal bleed – gastroduodenal artery

Question 310

Gastric disorders: Complications of PUD include:

1. Hemorrhage (MC)
2. Perforation
3. Gastric outlet obstruction

____ is the 2nd MC complication. It presents with sudden onset of severe, sharp, abdominal pain (generalized) with “acute abdomen”. Free air is seen on imaging.

Answer 310

Perforation

• acute abdomen: rigidity, guarding, rebound tenderness)
• free air

*can lead to: peritonitis, sepsis, hypotension, pancreatitis (if duodenal)

Question 311

Gastric disorders: Complications of PUD include:

1. Hemorrhage (MC)
2. Perforation
3. Gastric outlet obstruction

____ narrowing of the outflow tract due to edema/inflammation of the pylorus. It presents with early satiety, vomiting and weight loss.

Answer 311

Gastric outlet obstruction

*complications: dehydration, metabolic alkalosis

Question 312

Gastric disorders: _____ is a gram (-) curved rod that lives within the gastric mucosa (antrum).

It is transmitted by fecal-oral or oral-oral routes (organisms in stool or vomit). It acts by disrupting the mucous layer and liberating enzymes and toxins, making the mucosa more vulnerable to acid injury.

Answer 312

H. pylori. (MCC PUD)

may cause:

• asymptomatic
• -PUD
• -gastric atrophy (intestinal metaplasia/gastric carcinoma)
• -persistent stimulation of MALT (inc. risk gastric lymphoma)

Question 313

Gastric disorders: True/False - Chronic H. pylori gastritis is usually asymptomatic, however, in some cases, altered gastric secretion + tissue injury leads to PUD.

It may occasionally lead to gastric atrophy, intestinal metaplasia, and eventually gastric carcinoma.

Answer 313

True

*OR persistent stimulation of lymph may lead to gastric lymphoma

Question 314

Gastric disorders: True/False - Host immune response further perpetuates tissue injury in H. pylori infections.

The chronic inflammation induced by H. pylor upsets gastric acid secretory physiology to varying degrees.

Answer 314

True

Question 315

Gastric disorders: Which of the following is a mechanism that enables H. pylori to survive in the stomach?

a. flagella
b. urease
c. adhesins
d. exotoxins

Answer 315

A-C

flagella: swim to less acidic deep mucosa
ureas: urea – ammonia (inc. mucous pH)
adhesins: bind surface of gastric epithelial cells

Question 316

Gastric disorders: H. pylori uses urease to form ammonia which raises the pH, buffering the gastric tissue. The resulting host immune response (inflammation; gastritis) leads to injury. The bacterial enzymes also contribute to mucosal injury.

Finally, H. pylor stimulate the G-cells. How does this contribute to injury?

Answer 316

1. stimulate G cells in antrum
   - -infections predominate in antrum
   - -inc. gastrin release
2. gastrin stimulates parietal cells to secrete HCl
3. excess acid load injures duodenal mucosa (forming ulcers)

Question 317

Gastric disorders: There are 2 virulence factos present in some strains of H. pylori that are believed to contribute to inc. risk of complications (e.g. gastric carcinoma).

1. Cytotoxin-associated gene A (CagA)
2. Vacuolating cytotoxin A (Vac A)

Describe these virulence factors

Answer 317

1. CagA
   - -organisms injects into host cell
   - -interferes with cell processes (prolif. and diff. )
2. VacA
   - -secreted by organism
   - -interferes w/ cell pathways (inc. inflammation, intracell. vacuoles)

Question 318

Gastric disorders: True/False - In most patients, infection is limited to the antrum (inc. gastrin secretion and HCl production which increases duodenal ulcers).

However, in others, the entire stomach (pangastritis) may be involved. Over time, this results in destruction of gastric glands (gastric atrophy) which leads to hypochlorhydria (loss of parietal cells) and intestinal metaplasia.

Answer 318

True

*Gastric ulcers and carcinoma are associated with pangastritis pattern of infection

Question 319

Gastric disorders: H. pylori si present in nearly all patients with duodenal ulcers and most with gastric ulcers/chronic gastritis.

Treatment of H. pylori requires multiple drugs and confirmation of cure. Explain

Answer 319

1. Confirmation
   - -stool antigen test
   * if negative after 8 wks therapy, infection cured)
2. Treatment
   - -amox + clinda + PPI

Question 320

Gastric disorders: The choice of test used to Dx H. pylori depends on whether the patient requires an upper endoscopy.

Serologic detection of IgG abs is not often performed due to concerns over accuracy. Also, it does not distinguish b/t active and past infection. List tests used for H. pylori.

Answer 320

1. Biopsy for Histology
2. Biopsy urease test
   - -alkaline pH and color change if +
3. Urea breath test
   - -hydrolysis of urea by H. pylori – CO2 and NH3
   - -(+) = CO2 detected in breath samples
4. Stool antigen test
   - -(+) bacterial antigen = ongoing infection
   - -use to establish initial Dx and confirm eradication

Question 321

Motility drugs: Prokinetic drugs act to stimulate cholinergic neurons (and SM) thereby increasing contraction and propulsion.

There are 5 types/mechanisms:

1. M3 agonists
2. Ach inhibitors
3. Dopamine (D2) agonists
4. Motilin antagonists
5. Serotonin ….

List examples of each.

Answer 321

1. M3
   - -Bethenecal
2. Ach inhibitor
   - -Neostigmine
3. D2
   - -metoclopramide
   - -I.V.
   - -excreted unchanged by kidney
4. Motilin agonist
   - -erythromycin

Question 322

Motility drugs: The clinical uses for prokinetic drugs are to increase gastric tone and constrict sphincters/SM.

What are the adverse effects/contraindications associate with prokinetic drugs?

Answer 322

Administration:

• -oral
• -Metoclopromide: IV

Metabolism:
–hepatic (except metaclopromide)

Adverse:

1. cholinergic: parasympathomimetic
2. Dopamin: EPS/hyperprolactinemia

Question 323

Motlity drugs: Laxatives are drugs that are designed NOT to leave the intestine. They help to increase movement of fecal material. The following are the different kinds:

1. Emollient (mineral oil)
2. Saline (milk of Mg)
3. Castor oil
4. Psyllium (bulk forming)
5. Natural compounds (Senna, Frangula, Aloe, Rhubarb)

List their features

Answer 323

1. Emollient
   - -non-absorbed
   - -lubricates bowel
2. Saline
   - -inorganic salt
   - -inc. H2O into intestine (osmosis)
   * *fast, but explosive!!
3. Castor oil
   - -opens Cl- channels
   - -H20/electyolytes into intestine
4. Psyllium
   - -non-absorbable
   - -forms hydrophilic mass (dec. transit time; inc. H2O)
   * *safest, preferred
5. Natural
   - -contain antrhraquinone glycosides
   - -move H2o/electros into intestine; inc. fluid volume

Question 324

Motility drugs: What are the adverse effects of laxatives?

1. Secretory/stimulant agents
2. Saline
3. Mineral oil

Answer 324

1. Secretory
   - -electrolyte imbalance
2. Saline
   - -Mg absorption
   - -rectal epithelial sloughing
3. Mineral oil
   - -dec. absorption of fat-soluble vitamins
   - *pulmonary aspiration

Question 325

Motility drugs: Anti-diarrheal drugs are effective for “non-specific” diarrhea that is NOT attributed to bacterial infection. They are most effective for management of acute diarrhea.

The following are classes of anti-diarrheals:

1. opiates
2. anti-secretory agents
3. anti-cholinergics
4. gel-forming
5. ion exchanges resins

List examples of each and their functions.

NOTE: Most anti-diarrheal drugs act in the intestines (thus pharmacokinetics is not a factor.

Answer 325

1. opiates
   - -inc. flow resistance; dec. propulsion
   ex: loperamide (piperadine); diphenoxylate/atropine (phenylpiperadine)
2. anti-secretory
   - -dec. net fluid
   ex: bismuth salicylate
3. anti-cholinergics
   - -reduce contractile activity
   ex: dicyclomine
4. gel forming
   - -inc. flow resistance; inc. formed stools
   ex: hydrated silum silicate, pectin, kaolin
5. ion exchange resins
   - -bind bile water and salts
   ex: cholesteryramine

Question 326

Motility drugs: Opiate Anti-diarrheal agents (loperamide and Diphnoxylate) are given orally and are systemically-acting.

Descirbe absorption and metabolism of these agents

Answer 326

Absorption:

• Loperamide: poor
• Diphenoxylate: 90%

Metabolism:

• Loperamide: primarily biliary
• Diphenoxylate: hepatic

Question 327

Motlity drugs: Side effects of opiates Loperamide and Diphenoxylate is based on their abilities to diffuse across the Blood Brain Barrier.

Loperamide has minimal diffusion, and low abuse potential. What amount that does enter the brain is pumped out by P-gp. How does this compare to diphenoxylate?

Answer 327

–sufficient diffusion

Side effects:

• -Euphoria (atropine added to reduce abuse)
• -Respiratory depression (high doses) - naloxone reverses
• -if metabolized difenoxin (active metabolite - 200x more potent)

Question 328

Motility drugs: General points to treat poisoning include:

1. maintain vital functions
2. prevent further exposure
3. combat toxic effects
4. induce emesis

Syrup of Ipecac is an OTC emesis-inducing drug that can be used. It can cause local irritation and central CTZ stimulation. What are its contraindications?

Answer 328

• Corrosive acid or base = may aspirate
• CNS stimulants - inc. seizures
• Hydrocarbon = aspiration and chemical pneumonitis
• Activated charcoal = Ipecac (bind charcoal and neutralize both compounds)

Question 329

Motlity drugs: Ondansetron and Granisetron are anti-emetic drugs that act as _____ antagonists that are used to treat chemotherapy-induced emesis. Odensetron is also used for post-operative emesis.

They help to relieve nausea and vomiting due to anti-neoplastic therapy, and can be given by I.V. (1st pass).

Answer 329

5-HT3 antagonists

-P450 metabolism

Adverse:
–few (some anaphylactic w/ odensetron)

Question 330

Motility drugs: Metoclopramide and prochlorperazine are D2 Antagonists (anti-emetics) that are used in chemotherapy-induced emesis.

Their uses have declined with the development of 5HT3 antagonists, but are still used for less severe emesis. What are their side effects?

Answer 330

EPS and hyperprolactinemia

Question 331

Motility drugs: Other anti-emetics include

1. Dronabinol
2. Dimenhydrinate
3. Scopolamine

_____ is a chemotherapy-oinduced emesis when other drugs have failed. It has also been approved as an appetite stimulant in AIDS.

Answer 331

Dronabinol

Question 332

Motility drugs: Other anti-emetics include

1. Dronabinol
2. Dimenhydrinate and meclizine
3. Scopolamine

____ are H1 antagonists used for motion sickness

Answer 332

Demenhydrinate (dramamine) and meclizine (bonine)

Question 333

Motility drugs: Other anti-emetics include

1. Dronabinol
2. Dimenhydrinate
3. Scopolamine

Is an atropine-like muscarinic antagonist used to treat motion sickness

Answer 333

Scopolamine

Question 334

Gastric disorders: NSAIDS impair mucosal defense mechanisms by inhibiting cycloxegenase and thus decreasing prostaglandin production.

True/False - Decreased prostaglandin leads to direct mucosal injury due to decreased mucin and HCO3- secretion as well as decreased epithelial regeneration.

Answer 334

True

Question 335

Gastric disorders: Other factors that can lead to gastric injury include:

a. cigarette smoke
b. genetic predisoposition
c. blood group O

Answer 335

all of the above

1. cigarettes
   - -inc. PUD in smokers
   - -dec. healing rate (inc. free radicals and dec. duodenal HCO3-)
2. Genetic
   - -1st degree relative inc. risk (similar env. exposure)
3. Blood group O
   - -enhance binding of H. pylor

Question 336

Gastric disorders: H. pylor begins and often remains in the antrum. Over many years, the inflammation may extend and involve the more proximal stomach.

The associated injjury can cause patchy, atrophy (multi-focal atrophic gastritis) and lead to increased risk of metaplasia. It also lead to increased risk of malignant transformation to ________

Answer 336

adenocarcinoma

Question 337

Gastric disorders: Long standing H. pylori infection can spread to the fundus/body of the stomach (from the antrum) and cause autoimmune gastritis. This occurs by diffuse T-cell mediated destruction.

It leads to loss of ______cells, which results in achlorhydria (hypergastrinemia) and loss of IF (pernicious anemia).

Answer 337

loss of parietal cells

*Dx using antibodies to parietal cells and IF
not directly responsible for injury, but Dx

Question 338

Gastric disorders: Autoimmune T-cell mediated destruction of parietal cells due to long-standing H. pylori infection of the fundus and body (stomach).

Autoantibodies form against the parietal cell antigens and intrinsic factor. These autoabs are not pathogenic themselves, but are useful diagnostically.

Answer 338

Autoimmune gastritis

Complications:

1. destroy parietal cells
   - -loss of gastric acid
   - -inc. gastrin (negative feedback) = G-cell hyperplasia and inc. risk carcinoid tumors
   - -loss of IF = impaired B12 absorption = pernicious anemia
2. Long standing injury = intestinal metaplasia = adenocarcinoma

Question 339

Gastric disorders: A gastrin-secreting neuroendocrine tumor (gastrinoma) that is usually located in the duodenum or pancreas.

It increases gastrin secretion (inc. acid production). It is sporadic and often malignant.

Answer 339

Zollinger Ellison syndrome

Question 340

Gastric disorders: When should you suspect Zollinger ELlison?

a. multiple ulcers
b. ulcer resistant to therapy
c. family Hx of parathyroid or pituitary tumors
d. PUD + diarrhea (common)

Answer 340

all of the above

• Single ulcers in unusual locations (prox. duodenum)
• Multiple ulcers: distal duodenum or jejunum
• Ulcers resistant to therapy
• PUD + diarrhea
• Family Hx or parathyroid or pituitary tumors
• PUD without H. pylor or Hx of NSAIDS

Question 341

Gastric disorders: In patients with Zollinger Ellison syndrome, PUD may be multiple and more distal than the typical locations.

Alongside PUD, what other clinical associations may be found?

Answer 341

1. GERD
2. malabsorption
   - -inc. acid load in duodenum (inactivates pancreatic enzymes)
3. Liver = common site for metastasis from gastrinoma

*diarrhea, steatorrhea, weight loss

Question 342

Gastric disorders: Serum gastrin is used to diagnose Zollinger Ellison. Normal serum gastrin is <150 pg/ml.

1. Serum gastrin > 150: must measure gastric pH ratio to hyperchlorhydria. pH < 3 implies ______
2. If serum gastrin is equivocal (150-1000) do secretin stimulation test. Elevated levels of gastrin indicate ___.
3. Serum gastrin >1000 is diagnostic of _______.

Answer 342

1. hyperchlorhydria
   - -MC cause of elevated gastrin
2. possible gastrinoma
3. diagnostic of gastrinoma

• must take patients off H2 blockers and PPI’s to Dx
• Secretin test: Patients fast overnight – bolus of secretin next morning (IV) – measure gastrin

Question 343

Gastric disorders: A 45 year old male presents to the clinic compllaining of diarrhea and weight loss. You note ascites on PE.

Lab findings:

1. enlarged gastric rugae (cerebriform)
2. diffuse foveolar hyperplasia

What do you suspect?

Answer 343

Menetrier disease (hypertrophic gastropathy)

Question 344

Gastric disorders: Menetrier disease presents with weight loss, peripheral edema, and diarrhea.

It is due to excessive secretion of transforming growth factor A. Explain the MOA

Answer 344

1. Inc. TGFa
2. Overstimulate EGFR
3. mucous cells proliferate = fobeolar hyperplasia/excess mucous
4. loss of protein
   - –due to hypersecretion of gastric mucous
5. Edema

**possible increased risk for gastric cancer

Question 345

Gastric disorders: Gastric polyps include

1. ________: benign polyps that occur w/ gastritis, adjacent to ulcers and erosions.
2. _______: sporadic polyps that are commonly produced from proton pump inhibitors (omeprazole). Inhibiting acid production – hypergastrinemia and stimulation of fundic glands.
3. _______: Dysplastic with potential for malignant transformation (especially w/ increased size > 2cm). Increased incidence in familial adenomatous polyposis.

Answer 345

1. Hyperplastic polyp
2. Fundic gland polyp
   - -familial adenomatous polyposis
3. Gastric adenoma

Question 346

Gastric disorders: A benign SM tumor that most often occurs in the stomach.

It may ulcerate or bleed, but has NO malignant potential

Answer 346

Leiomyoma

MC benign soft tissue tumor in the stomach

Question 347

Gastric disorders: Most gastric malignancies are gastric adenocarcinoma.

Risk factors include:

a. H. pylor
b. autoimmune gastritis
c. blood group A
d. high intake of salt-preserved foods and smoked meats

Answer 347

all of the above

*familial pre-disposition (hereditary diffuse gastric cancer - CDH1 gene mut.)

NOTE: dec. incidence in U.S. due to refrigeration

Question 348

Gastric disorders: The “Intestinal” type of gastric adenocarcinoma is decreasing in incidence (due to dec. prevalence of H. pylori and dec. ingestion of dietary carcinogens due to refrigeration).

It is causally related to H. pylor in that, over time, inflammatory infiltrate leads to loss of original gastric glands (atrophic gastritis). Thus multi-focal atrophy may be followed by intestinal metaplasia. What does this lead to?

Answer 348

Hyperchlorhydria
—atrophic and metaplastic glands replace original glands and inc. acid production

*unstable epithelium = inc. risk dysplasia and malignancy

Question 349

Gastric disorders: A patient you know has gastric adenocarcinoma.

This type arises from intestinal metaplasa, forms an exophytic mass, and resembles intestinal cancer (forms glands).

Answer 349

Intestinal type

Question 350

Gastric disorders: This type of gastric adenocarcinoma is NOT associated with H. pylori. It is associated with diffuse thickining of the gastric wall (w/ no distinct mass).

On histology, you note diffuse infiltration of the wall and “signet ring” cells.

Answer 350

Diffuse type

• signet ring = mucin vacuole that displaces nucleus to the side
• pathogenesis: inactivation of CDH1 (encodes cadherin) = inc. tumor growth and invasion

Question 351

Gastric disorders: The diffuse type of gastric adenocarcinoma is caused by loss of CDH1 gene that encodes E-cadherin.

E-cadherin is a cell surface protein that is involved with intercellular connections. Loss of this protein leads to loss of adhesion molecules and permits growth and invasion of tumor cells. What are clinical features of the diffuse type?

Answer 351

• high incidence of metastasis
• rapid disease progression
• poor prognosis

Question 352

Gastric disorders: Weight loss and abdominal pain are the MC symptoms of gastric cancer at diagnosis.

Dysphagia is common in those with tumors arising in the _________.

Patients may also present with signs/symptoms of distant metastasis in the liver, peritoneal surfaces, and lymph nodes

Answer 352

dysphagia: proximal stomach and esophagogastric jxn

Question 353

Gastric disorders: True/Fase - Common metastasis sites of gastric adenocarcinoma include

1. Virchow node (left supraclavicular)
2. Periumbilical subcutaneous tissue (Sister Mary Joseph nodule)
3. Bilateral ovaries (Krukenberg tumor; signet ring type)

Answer 353

True

Question 354

Gastric disorders: Velvety dark plaques on the axilla, and posterior neck. They are commonly associated with gastric adenocarcinoma.

Answer 354

Acanthosis nigrans

*not specific for malignancy, but if malignancy is present, it is MC gastric cancer

Question 355

Gastric disorders: True/Fasle - Multiple seborrheic keratosis (sign of Leser trelat) is a paraneoplastic manifestation associated with gastric adenocarcinoma

Answer 355

True

Question 356

Gastric disorders: Treatment of gastric adenocarcinoma involves surgical resection.

Prognosis depends on stage (depth of invasion, extend of nodal and/or distant metastasis).

True/False - stage of tumor increases with increasing depth of invasion into the gastric wall

Answer 356

true

Question 357

Gastric disorders: Gastric lymphoma is the MC extranodal site of lymphoma. Most are extranodal marginal zone B-cell lymphoma (MALToma). However, less commonly, we see diffuse large B cell lymphoma.

MALToma is a type of low grade B cell lymhoma that is related to chronic stimulation of MALT by ______.

Answer 357

H. pylori

• Tx infection = lymphoma resolves
• non-specific clinical features

Histo: dense, lymphocytic infiltrate w/ lymphoepithelial lesions

Question 358

IBS drugs: _______ can be used to Tx traveller’s diarrhea. It is similar to rifamycin. Little absorption, so most of the drug remains in the intestine (site of action

Answer 358

Rifaximin (XIFAXAN)

Question 359

IBS drugs: Drugs to treat inflammatory bowel include:

1. Aminosalicylates (5-ASA)
2. Steroids (Glucocorticoids; anti-inflammatory)
3. Immune modifiers (Azathioprine, 6-MP, methotrexate)
4. Biologic therapy (Infliximab)
5. Antibiotics (metronidazole, ampicillin, cipro)
6. Non-drug treatment therapy (surgery; MC Crohn’s)

How do you treat an IBS patient with unknown causes?

Answer 359

Tx symptoms

• dietary changes, stress manamegment
• pharm varies patient to patient – can be difficult

Question 360

IBS: The current (standard) approach is to treat “bottom up” according to severity of the illness. The bottom up approach involves:

1. mild: antibiotics, salicylates
2. moderate: immunomods and corticosterods
3. biologics

Hows does this compare with the newer “top down” approach?

Answer 360

Treat early to late stages

1. Early
   - -immunomodulators/biologics
2. Middle
   - -immunomods + corticosteroids + aminosalicylates
3. Late
   - -immunomods
   - -surgery or antibiotics or aminosalicylates

Question 361

IBS: Aminosalicylates include: Sulfasalazine (5 ASA), Olsalazine balsalazine (and forms of mesalamine). These drugs form AZO bonds with other molecules to prevent absorption of the 5 ASA parent compound in the small intestine, thus allowing the drug to enter the large intestine and enabling remission in UC.

Answer 361

True

1. Sulfasalazine
   - -Sulfapyridine linked to 5 ASA (mesalamine) by AZO bond
   - -sulfapyridine (rapid absorption in colon - no therapy)
2. Balsalazide
   - -5 ASA + 4 aminobensoyl-B alanine
3. Olsalazine (diaminosalicylate)
   - -2 5 ASA molecules together
   - -broken down by intestinal bactera to form 2 5-ASA’s

Question 362

IBS: What is the Mechanisms of action of Salicylates (sulfsalazine, olsalazine)?

a. inhibit prostaglandin synthesis via inhibition of COX-1
b. inhibit cell function of NK cells, lymphocytes and macrophages
c. scavenge free radicals and prevent oxidative damage
d. inhibit NF-KB

Answer 362

All

• inhibit COX (PG biosynthesis),
• -tf for pro-inflamma cytokines
• -inhibit IL-1 and TNF-a
• -inhibit NFK-B
• -inhibit cell fxn of NK cells, lymphocytes, macros
• -scavenge free radicals/prevent ox damage

Question 363

IBS: Mesalamine (5ASA) is the active metabolite of salycilates. Mesalamine-only formulations include:

1. Pentasa
2. Asacol
3. Enema or Suppository

How do they work?

Answer 363

1. Pentase
   - -time release micro-granules (throughout SI)
2. Asacol
   - -coated 5 ASA
   - -dissolves at pH 7 (ileum and colon)
3. Enema
   - -5 ASA may be delivered in high conc. (sigmoid colon)

Question 364

IBS: Salicylates are used to maintain remission in UC. Efficacy is unknown in Crohn’s disease (more efficacious in UC). Efficacy in Crohn’s is dependent upon the site of inflammation (SI vs. LI) and confined to use of the suppository.

If the disease extends to the proximal colon (UC or Crohn’s) what formulations can be used?

Answer 364

AZO and meslamine

Question 365

IBS: What are the side effects of salicylates?

Answer 365

1. Sulfasalazine (releases sulfapyridine)
   - -nasua, bone marrow suppression, GI uupset
   - -ulfonamides – hemalytic anemia or hepatitis
2. Osalazine
   - -secretory diarrhea
3. Mesalamine (high doses)
   - -interstitial nephritis

Question 366

IBS: Glucocorticoids act to:

1. inhibit formation of inflammatory cytokine (TNF alpha, IL-1) and chemokine (IL-8)
2. reduce the expression of inflammatory cell adhesion molecules,
3. inhibit gene transcription of NO synthase, phospholipase A2, COX-2, NF-Kb

They are NOT useful at maintaining remission. What are their clinical uses?

Answer 366

1. Prednisone/Prednisolone
   - -intermediate
   - -orally
2. Hydrocortisone
   - -fast acting steroid
   - -enema, foam suppository
   - -minimize systemic glucocorticoid effect
3. Budesonide
   - -time release (distal ileum/colon)
   - -Tx moderate to severe inflammatory bowel

Question 367

IBD: What are the side effects of glucocorticoids with respect to:

1. bone
2. gut
3. glucose
4. CNS

Answer 367

1. Inc. bone absorption
   - -alter Ca2+ handling
   * *children; post-menopause
2. Inc. peptic ulcer
   - -inc. acid production
   - -dec. mucopolysaccharides
3. Hyperglycemia (DM)
   - -a. inc. gluconeogenesis and secretion by liver; sensitivity to glucagon; substrate for gluconeogenesis
   - -b. dec. glucose uptake by peripheral tissues
4. Inc. arousal and euphoria
   - -prolonged = depression/sleep issues/psychosis

Question 368

IBD: Purine analogs include purine anti-metabolites (Azathiopurine and 6-mercaptopurine).

They are immunosuppressive drugs that are believed to act by enhancing apoptosis of T-lymphocytes and inhibiting cell division and proliferation (by inhibiting nucleotide metabolism).

Describe these drugs

Answer 368

1. Azathopurine
   - -bioavailability better than mercaap.
   - -converted non-enzymatically to 6-MP
2. 6MP
   - -metabolized by xanthine oxidase and thiopurine methyltransferase to: thioguanine or inactive metabs.
   * *long half life (delays azathoprine effect to 17 weeks)

Question 369

IBD: Purine analogs are used for induction and maintenance of remission (UC and Crohn’s after 3-6 mos Tx). They maintain remission in ~80% of patients.

When administered for long durations, steroid doses must be reduced. What are their adverse effects?

Answer 369

1. nausea, vomiting bone marrow suppression
   - -leukopenia, anemia thrombocytopenia
   - -leukopenia responds to dose reduction or GSF
   * must monitor Thioguanine levels (TMT defciency inc. bone marrow suppression)
2. Hypersensitivity reactions
   - -pancreatitis, hepatitis, fever

Question 370

IBD: Purine analogs can have drug interactions with Allopurinol.

Allopurinol reduces the activity of xanthine oxidase, decreasing the metabolism of purine analogs. What is the net result?

Answer 370

High thioguanine = leukopenia

Fix by reducing dose of azathioprine (when taking allopurinol)
*~50% of normal dose

Question 371

IBD: Methotrexate is an anti-metabolite used to treat chronic inflammatory diseases (Crohn’s, RA, Cancer).

It inhibits dihydrofolate reductase (DHF reductase) which is essential for synthesis of thymidine and purines.

How is it used clinically?

Answer 371

1. Cancer - high doses
   - -inhibit cell prolifer.
2. Interferes with inflammation
   - -via IL-1
3. Stimulates relase of adenosine
   - -anti-inflamm
4. may induce death of T-cells

Question 372

IBD: Methotrexate is used to induce and maintain remission in Crohn’s. It’s efficacy in UC is unknown.

What are adverse effects associated with methotrexate?

Answer 372

1. Low incidence:
   - -bone marrow suppression, alopecia, mucositis, megaloblastic anemia

*uncommon

IF side effects occur - reduce dose and give folic acid

Question 373

Biochem: A kid who presents with decreased eye contact, exaggerated startle response, hyperreflexia and maculae with a cherry red spot.

Labs reveal onion skin lysosomes (labs)

most likely has a deficiency in

Answer 373

B hexosaminidase

*Tay sachs (accumulate G2 ganglioside)

• -**regression of achieved milestones
• -neurodegeneration (macroencephaly, difficulty moving), developmental delay,

Question 374

Biochem: A kid who presents with recurrent pneumonia, hepatosplenomegaly, cherry red maculae.

Foam cells prsent in bone marrow, spleen and liver. Zebra bodies (myelinated membranes (parallel palisading laminae)

Answer 374

Niemann Pick

*sphingomyelin accumulation (def. sphingomyelinase)

Question 375

Biochem: A patient presents with glomerulonephritis, hematuria and sensorineural hearing loss.

Ocular findings include anterior lenticonus.

Labs reveal:

1. Microhematuria
2. Splitting of the glomerular BM (basketweave) on biopsy

*can’t pee, can’t see, can’t hear a bee

Answer 375

Alport Syndrome

• Mutation in type IV collagen
• end stage renal disease

Question 376

Biochem: A kid who presents with osteoporosis, pancytopenia, bone crises, avascular necrosis and hepatosplenomegaly.

Labs reveal lipid-laden macrophages that look like tissue paper

Answer 376

Gaucher disease

def. B-glucocerebroside
* glucocerebroside accumulation
* Gaucher cells

Tx: recombinant glucocerebroside

Question 377

Biochem: A patient who presents with black pigmented tissues

Answer 377

Alkaptonuria

*dec. B-homogentisate oxidase

Pixorize: “Owl captain” uria

Question 378

Biochem: A patient who presents with a protuberant abdomen, puffy cheeks, rounded face…

Labs reveal severe hypoglycemia, lactic acidosis and hyperuricemia (gout).

Answer 378

Von Gierke

*dec. gluc 6-phos translocase

Question 379

Biochem: A patient presents with developmental delay, delayed language development, long facies, large ears, macrochordism (testicular enlargement) and mitral valve prolapse.

Joints are hypermobile and pes planus.

Answer 379

Fragile X

• X-linked dominant
• trinucleotide repeat FMR1 gene
• inc. methylation

Question 380

Biochem: A patient presents with maple syrup/burnt sugar smelling urine

Answer 380

Maple syrup urine disease

*Leucin

Question 381

Biochem: patient presents with almond shaped eyes, turned down mouth, and increased appetite

Answer 381

15q11q13

*mutation of paternal (microdeletion)

Question 382

Biochem: Patient presents with thin upper lip, receding chin and smooth philtrum

Answer 382

fetal alcohol syndrome

Question 383

Biochem: Patient presents with hypotonia, abnormal facial grimacing, hepatomegaly

Answer 383

Zellweger syndrome

*absence of peroxisomes

Question 384

Biochem: A child (6-18 mos) presents with regression of motor skills, speech and cognition.

On PE you note vocal grunting and hand wringing

a. Rett
b. Krabbe
c. Puetz Jegher
d. Williams

Answer 384

Rett syndrome

• X-linked dominant
• microdeletion of methyl CPG binding protein 2
• progressive loss of intelligence, cognition (language, motor)
• females

Question 385

Biochem: A patient presents with neuropathies, limb stiffness and optic atrophy

Lab reveals globoid cells

Answer 385

Krabbe disease

*def. galactocerebrosidase

Question 386

Biochem: A patient present with angiokeratomas, burning pains in his hands and feet and foamy urine

a. Fabry
b. Rett
c. Cri-du Chat
d. Gaucher

Answer 386

Fabry

X-linked recessive
*def. a-galactosidase A