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GI Flashcards

1
Q

What is considered the foregut, midgut and hindgut?

A
  • the foregut is the pharynx to the duodenum, including the liver, gallbladder, pancreas, and spleen
  • the midgut is the duodenum to the proximal ⅔ of the transverse colon
  • the hindgut is the ⅔ of the transverse colon to the pectinate line
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2
Q

Describe midgut development in utero.

A
  • around week 6, the midgut herniates through the umbilical ring
  • around week 10, it returns to the abdominal cavity while rotating around the SMA
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3
Q

What is gastroschisis?

A

this is a ventral wall defect that arises from failure of the abdominal folds to properly close, leaving the abdominal contents exposed

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4
Q

What is an omphalocele?

A
  • this is a ventral wall defect that arises from persistent herniation of the abdominal contents into the umbilical cord
  • the result is that the abdominal contents remain outside the body but are covered by the peritoneum and amnion of the umbilical cord
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5
Q

How does a gastroschisis differ from an omphalocele?

A

gastroschisis leaves the abdominal contents in the abdomen and exposed while omphalocele leaves them herniated and covered by the peritoneum

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6
Q

What is the most common tracheoesophageal anomaly?

A

esophageal atresia with distal tracheoesophageal fistula

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7
Q

How does a pure esophageal atresia/stenosis differ from an EA with distal TEF?

A
  • in those with a TEF, air is able to enter the stomach

- in those with no TEF and atresia alone, this doesn’t occur and there is a gasless abdomen

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8
Q

Esophageal Atresia with Distal Tracheoesophageal Fistula

A
  • the most common TE anomaly
  • presents with polyhydramnios in utero
  • neonates drool, choke, and vomit at the time of their first feeding
  • the TEF allows air to enter the stomach and duodenum; this helps differentiate it from esophageal atresia alone
  • cyanosis can occur secondary to laryngospasm, which occurs to avoid reflux-related aspiration
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9
Q

Duodenal Atresia

A
  • failure of the duodenum to canalize
  • presents with polyhydramnios in utero plus bilious vomiting and abdominal distention within the first 1-2 days of life
  • dilation of the stomach and proximal duodenum occurs and has a “double bubble” appearance on x-ray
  • strongly associated with Down syndrome
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10
Q

Jejunal/Ileal Atresia

A
  • failure of parts of the jejunum or ileum to develop due to distruption of the SMA
  • leads to ischemic necrosis and segmental resorption of the affected segment
  • affected segment takes on a spiraled, “apple peel” appearance
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11
Q

Hypertrophic Pyloric Stenosis

A
  • congenital hypertrophy of pyloric smooth muscle
  • the most common cause of gastric outlet obstruction in infants; more common in males
  • presents with non-bilious, projective vomiting at 2-6 weeks old (begins developing at time of birth), which contributes to a hypokalemic, hypochloremic metabolic alkalosis
  • can be palpated as an “olive” like mass in the epigastric region and you can visualize peristalsis
  • more common in first born males and associated with exposure to macrolides
  • treatment is surgical
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12
Q

Describe development of the pancreas.

A
  • it is derived from the foregut, which gives rise to two pancreatic buds
  • the ventral bud contributes to the uncinate process and main pancreatic duct
  • the dorsal bud becomes the body, tail, isthmus, and accessory pancreatic duct
  • both buds contribute to the head
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13
Q

What is the Ampulla of Vater?

A
  • the dilated portion of the main pancreatic duct where the gall bladder drains into
  • terminates in the sphincter of Odi within the duodenal wall
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14
Q

Annular Pancreas

A
  • a ventral pancreatic bud abnormality
  • arises as the ventral bud encircles the 2nd part of the duodenum
  • presents with non bilious vomiting and abdominal dissension, much like duodenal atresia
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15
Q

Pancreas Divisum

A
  • failure of the ventral and dorsal pancreatic buds to fuse
  • relatively common and most often asymptomatic
  • may cause chronic abdominal pain and/or pancreatitis
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16
Q

Which abdominal structures are retroperitoneal?

A

SAD PUCKER

  • suprarenal glands
  • aorta and IVC
  • duodenum (2nd-4th parts)
  • pancreas (except tail)
  • ureters
  • colon (descending and ascending)
  • kidneys
  • esophagus (thoracic portion)
  • rectum (in part)
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17
Q

Where is the falciform ligament? What runs within it?

A
  • it is the ligament that connects the liver to the anterior abdominal wall
  • contains the ligament teres hepatic derived from the fetal umbilical vein
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18
Q

What is contained within the hepatoduodenal ligament?

A

the portal triad (proper hepatic artery, portal vein, and common bile duct)

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19
Q

What is the Pringle maneuver?

A

a maneuver that consists of compressing the hepatoduodenal ligament, and the portal triad within, by placing your thumb and index fingers within the omental foramen to control bleeding

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20
Q

What runs in the gastrohepatic ligament?

A

gastric arteries

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21
Q

Where is the gastrocolic ligament and what runs within it?

A
  • it connects the greater curvature of the stomach with the transverse colon as part of the greater omentum
  • it contains gastroepiploic arteries
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22
Q

What two ligaments separate the greater and lesser peritoneal sacs?

A
  • gastrohepatic

- gastrosplenic

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23
Q

What runs within the gastrosplenic ligament?

A
  • short gastric arteries

- left gastroepiploic vessels

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24
Q

What does the splenorenal ligament contain?

A
  • the splenic artery and vein

- the tail of the pancreas

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25
Q

What are the layers of the gut tube?

A
  • mucosa (epithelium, BM, lamina propria)
  • submucosa ( + Meissner plexus)
  • muscularis externa (inner circular, Auerbach plexus, outer longitudinal)
  • serosa/adventitia (intraperitoneal/retroperitoneal)
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26
Q

What is the basal rate of slow waves in the stomach, duodenum, and ileum?

A
  • stomach: 3 per minute
  • duodenum: 12 per minute
  • ileum: 8-9 per minute
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27
Q

What epithelium lines the esophagus?

A

a non-keratinized stratified squamous epithelium

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28
Q

What are Brunner glands?

A

glands found in the submucosa of the duodenum, which secrete bicarbonate and serve to protect the duodenum from gastric acid

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29
Q

At what vertebral level do the celiac trunk, SMA, and IMA branch off of the abdominal aorta?

A
  • celiac: T12
  • SMA: L1
  • IMA: L3
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30
Q

Superior Mesenteric Artery SYndrome

A
  • a syndrome of intermittent intestinal obstruction
  • associated with diminished mesenteric fat (e.g. low body weight or malnutrition)
  • the transverse duodenum is compressed between the SMA and aorta
  • primary symptom is post-prandial pain
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31
Q

Where do the foregut, midgut, and hindgut receive their blood supply and parasympathetic innervation?

A
  • foregut: celiac trunk, vagus nerve
  • midgut: SMA, vagus nerve
  • hindgut: IMA, pelvic nerve
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32
Q

Describe the vasculature that arises from the celiac trunk.

A
  • the trunk gives rise to the common hepatic, splenic, and left gastric arteries:
  • the common hepatic then gives rise to the proper hepatic (which ascends before giving off the right gastric) and the gastroduodenal artery, which divides into the right gastroepiploic artery and pancreaticoduodenal arteries
  • the left gastric gives off an ascending esophageal branch before running along the lesser curvature and forming a strong anastomosis with the right gastric
  • the splenic artery supplies the renal artery but also gives rise to the short gastric arteries that supply the fundus and the left gastroepiploic artery
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33
Q

Between what vessels do varices form as a result of portal hypertension? What is the clinical manifestation of each?

A
  • esophageal varices: left gastric anastomoses with the azygos
  • caput medusae: paraumbilical veins with the small epigastric veins of the anterior abdominal wall
  • anorectal varices: superior rectal with the middle and inferior rectal veins
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34
Q

What is a transjugular intrahepatic portosystemic shunt?

A

a shunt placed between the portal vein and hepatic vein to relieve portal hypertension

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35
Q

What is the pectinate line?

A

a line formed by the meeting of the endoderm and ectoderm in the anal canal

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36
Q

How does the region of the anal canal above the pectinate line differ from that below it in blood supply, venous drainage, lymphatic drainage, possible pathologies, and innervation?

A
  • above: risk of internal hemorrhoids (painless) and adenocarcinoma; supplied by the superior rectal artery from the IMA; and drained into the portal system via the superior rectal vein and IMV; drains to the internal iliac nodes
  • below: risk of external hemorrhoids (painful), anal fissures, and squamous cell carcinoma; supplied by the inferior rectal artery from the internal pudendal artery; and drained into the internal iliac and IVC directly via the inferior rectal and internal pudendal veins; drains to the superficial inguinal nodes
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37
Q

Anal Fissure

A
  • a tear in the anal mucosa below the pectinate line
  • most often posteriorly because that is the most poorly perfused area
  • associated with low-fiber diets and constipation
  • presents with pain while pooping and blood on toilet paper
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38
Q

Where are Kupffer cells located? What is their role?

A
  • they are specialized macrophages found in the liver

- they line the sinusoids

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39
Q

Where are stellate cells found? What is their role?

A
  • also known as ito cells, they are found in the space of disse, the perisinusoidal space of the liver
  • they store vitamin A when quiescent and are responsible for liver fibrosis when activated
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40
Q

Describe the direction of blood and bile flow through the liver?

A
  • blood flows from zone I to III from the portal vein/hepatic artery to the central vein
  • bile flows in the opposite direction
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41
Q

What is unique about zone I of the liver?

A
  • the area surrounding branches of the portal vein and hepatic artery
  • the first zone affected by viral hepatitis and ingested toxins
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42
Q

What is unique about zone II of the liver?

A

it is the most affected by yellow fever

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43
Q

What is unique about zone III of the liver?

A
  • the area surrounding the central vein
  • the first affected by ischemia
  • contains the P450 system
  • most sensitive to metabolic toxins
  • the site of alcoholic hepatitis
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44
Q

What structures are found within the femoral region and in what order are they situated?

A
  • from lateral to medial (toward the navel) you will find the nerve, artery, vein, and then lymphatics (NAVeL)
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45
Q

What structures form the femoral triangle?

A
  • the inguinal ligament superiorly
  • the sartorius muscle laterally
  • the adductor longs muscle medially
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46
Q

What structures are contained within the femoral sheath?

A

the vein, artery, and canal (containing the deep inguinal lymph nodes)

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47
Q

What structures normally passes through the inguinal canal in males and females?

A

the spermatic cord in males and the round ligament of the uterus in females

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48
Q

What are the two primary complications of hernias?

A
  • incarceration (not reducible)

- strangulation (ischemia and necrosis)

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49
Q

On which side are diaphragmatic hernias more common?

A

the left because the right is relatively protected by the liver

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50
Q

What is the most common kind of diaphragmatic hernia?

A

a hiatal hernia in which the stomach herniates upward through the esophageal hiatus

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51
Q

What is a sliding hiatal hernia?

A
  • the most common diaphragmatic hernia

- it results when the gastroesophageal junction is displaced upward, forming a “hourglass stomach”

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52
Q

What is a paraesophageal hernia?

A

a type of herniation of the stomach through the esophageal hiatus in which the gastroesophageal junction is in it’s normal location but the fundus of the stomach protrudes into the thorax next to the esophagus

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53
Q

Indirect Inguinal Hernia

A
  • a hernia that begins with tissue entering the internal inguinal ring lateral to the inferior epigastric vessels
  • goes through the internal inguinal ring, through the external inguinal ring, and into the scrotum
  • follows the path of descent of the testes and is covered by all three layers of the spermatic fascia (internal, cremasteric, external)
  • occurs in infants due to failure of the processes vaginalis to close, particularly in males
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54
Q

Direct Inguinal Hernia

A
  • a hernia that bulges directly through the abdominal wall, through the inguinal triangle (medial to the inferior epigastric vessels, lateral to the rectus abdominis, superior to the inguinal ligament)
  • it passes through the external inguinal ring only and protrudes through the inguinal triangle
  • it is covered only by the external spermatic fascia
  • it is more prevalent in older men
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55
Q

What kind of abdominal hernia is most common in infants, older men, and older women?

A
  • infants: indirect inguinal hernia
  • men: direct inguinal hernia
  • women: femoral hernia
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56
Q

Where are indirect inguinal, direct inguinal, and femoral hernias located?

A
  • indirect: above the inguinal ligament, lateral to the inferior epigastric vessels
  • direct: above the inguinal ligament in the inguinal triangle medial to the inferior epigastric vessels
  • femoral: below the inguinal line, lateral to the pubic tubercle
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57
Q

Describe the source, action, and regulation of gastrin.

A
  • secreted by G cells in the antrum of the stomach and duodenum
  • in response to stomach distention or alkalization, amino acids, vagal stimulation via gastrin-releasing peptide
  • promotes gastric acid secretion, growth of gastric mucosa, and gastric motility
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58
Q

Gastrin levels will rise if what medication is used chronically?

A

PPI

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59
Q

How do gastrin levels change in chronic atrophic gastritis?

A

they increase

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60
Q

Describe the source, action, and regulation of somatostatin.

A
  • secreted by D cells in the pancreatic islets and GI mucosa
  • in response to an increase in acid or decrease in vagal stimulation
  • serves to decrease gastric acid and pepsinogen secretion, pancreatic and small intestine fluid secretion, gall bladder contraction, and insulin and glucagon release
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61
Q

What is octreotide? What are it’s primary uses and adverse effects?

A
  • a somatostatin analog used to treat acromegaly, carcinoid syndrome, and variceal bleeding
  • may cause nausea, cramps, steatorrhea, or cholelithiasis
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62
Q

Describe the source, action, and regulation of CCK.

A
  • secreted by I cells in the duodenum and jejunum
  • in response to an increase in fatty acids or amino acids
  • increases pancreatic secretion and gallbladder contraction, slows gastric emptying, and relaxes the sphincter of Odi
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63
Q

Describe the source, action, and regulation of secretin.

A
  • secreted by S cells in the duodenum
  • in response to an increase in acid or fatty acids in the lumen of the duodenum
  • increases bicarb secretion from the pancreas, lowers gastric acid secretion, and increases bile secretion
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64
Q

Give two reasons bicarb secreted by the pancreas is important.

A
  • it helps neutralize gastric acids, protecting the small intestine
  • it neutralizes the gastric acid, which is necessary for pancreatic enzymes to function
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65
Q

Describe the source, action, and regulation of glucose-dependent insulinotropic peptide.

A
  • also known as GIP, it is secreted by K cells in the duodenum and jejunum
  • in response to fatty acids, amino acids, or oral glucose
  • stimulates insulin release and reduces gastric acid secretion
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66
Q

Why does oral glucose lead to a greater release of insulin than a the equivalent dose of glucose IV?

A

because oral glucose triggers release of GIP (glucose-dependent insulinotropic peptide/gastric inhibitory peptide), which stimulates additional insulin release

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67
Q

Describe the source, action, and regulation of motilin.

A
  • secreted within the small intestine
  • in response to a fasting state
  • produces migratory motor complexes
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68
Q

What is the clinical use of motilin agonists?

A

they are used to stimulate intestinal peristalsis

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69
Q

Describe the source, action, and regulation of vasoactive intestinal polypeptide.

A
  • secreted by parasympathetic ganglia in sphincters, gallbladder, and small intestine
  • in response to distention, vagal stimulation, and reduced adrenergic input
  • serves to increase intestinal water and electrolyte secretion (i.e. VIPomas cause a watery diarrhea) as well as relaxation of intestinal smooth muscle and sphincters
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70
Q

What are the symptoms of a VIPoma?

A

symptoms are derived from it’s action of increasing water and electrolyte secretion in the small intestine and relaxing sphincters

  • watery diarrhea
  • hypokalemia
  • achlorhydia
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71
Q

Describe the source, action, and regulation of gherlin.

A
  • secreted by cells in the stomach
  • in response to fasting
  • stimulates appetite
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72
Q

What molecule is responsible for mediating smooth muscle relaxation within the GI tract and of the LES?

A

nitric oxide

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73
Q

Describe the source, action, and regulation of intrinsic factor.

A
  • produced by parietal cells in the stomach

- binds VitB12 and required for VitB12 absorption in the terminal ileum

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74
Q

Describe the source and regulation of gastric acid secretion.

A
  • secreted by parietal cells in the stomach
  • promoted by histamine, ACh, and gastrin
  • inhibited by somatostatin, GIP, prostaglandin, and secretin
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75
Q

Describe the source, action, and regulation of pepsin.

A
  • secreted by chief cells in the stomach as pepsinogen, which is activated by gastric acid
  • in response to vagal stimulation and local acid
  • aids in protein digestion
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76
Q

Describe the source, action, and regulation of bicarb secretion within the GI tract.

A
  • secreted by mucosal cells in the stomach, duodenum, salivary glands, and pancreas as well as from Brunner glands in the duodenum
  • largely basal secretion, but increased release from pancreas and gall bladder in response to secretin
  • to neutralize acid
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77
Q

How does gastrin induce gastric acid release?

A

it has some direct effect on parietal cells in the stomach, but primarily it acts on enterochromaffin-like cells, which then secrete histamine onto parietal cells

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78
Q

What three vitamin/mineral deficiencies are of concern in those with small bowel disease or who have had a resection?

A
  • iron
  • folate
  • B12
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79
Q

Where and in what form is iron absorbed in the GI tract?

A

absorbed as Fe 2+ from the duodenum

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80
Q

Where is folate absorbed along the GI tract?

A

the small intestine

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81
Q

Where is B12 absorbed along the GI tract?

A

the terminal ileum

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82
Q

Where in the GI tract are bile salts re-absorbed?

A

the terminal ileum

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83
Q

What is intrinsic factor necessary for?

A

the absorption of vitamin B12 in the terminal ileum

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84
Q

List the three groups of pancreatic enzymes that are secreted.

A
  • a-amylase
  • lipases
  • proteases
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85
Q

How does an increase or decrease in the flow of pancreatic secretions change the content of the solutions?

A
  • low flow secretions have a high chloride ion content

- high flow secretions have a high bicarb content

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86
Q

What is unique about alpha-amylase secreted by the pancreas?

A

it is the only enzymes that is secreted active form

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87
Q

Describe pancreatic enzyme activation.

A
  • alpha-amylase is secreted in the active form
  • enterokinase/enteropeptidases in the brush-border of the duodenum and jejunum activate trypsin, which then activates the rest of the pancreatic proenzymes
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88
Q

What is the first pancreatic protease activated? How is it activated?

A

trypsin is the first activated and it is activated by enterokinases and enteropeptidases in the brush-bord of teh duodenum and jejunum

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89
Q

Enterocytes are capable of absorbing what carbohydrates?

A

only monosaccharides (e.g. glucose, galactose, and fructose)

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90
Q

Describe how glucose gets from the lumen of the small intestine into the blood.

A
  • via the Na-dependent SGLT1 from the lumen into enterocytes

- then into the blood by GLUT-2

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91
Q

Describe how galactose gets from the lumen of the small intestine into the blood.

A
  • via the same Na-dependent SGLT1 as glucose into enterocytes
  • then into the blood by GLUT-2
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92
Q

Describe how fructose gets from the lumen of the small intestine into the blood.

A
  • into enterocytes via facilitated diffuse mediated by GLUT-5
  • then into the blood by GLUT-2
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93
Q

What is the D-xylose absorption test?

A
  • a test used to distinguish GI mucosal damage from other causes of malabsorption
  • it is a monosaccharide and passively absorbed thus only requires an intact mucosa for absorption
  • in those with a mucosal defect or bacterial overgrowth blood and urine levels remain low; but in those with pancreatic insufficency, blood and urine levels rise normally
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94
Q

Describe the location, structure, and primary cell types of Peyer’s patches.

A
  • they are unencapsulated lymphoid tissue aggregates found in the lamina porpria and submucosa of the ileum
  • M cells sample the lumen and present antigens to B cells, which differentiate into IgA-secreting plasma cells
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95
Q

What is bile composed of?

A
  • bile salts (acids conjugated to glycine or taurine)
  • phospholipids
  • cholesterol
  • bilirubin
  • water and ions
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96
Q

What enzyme catalyzes the rate-limiting step of bile acid synthesis?

A

cholesterol 7a-hydroxylase

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97
Q

List three functions of bile.

A
  • promote digestion and absorption of lipids and fat-soluble vitamins
  • cholesterol excretion
  • antimicrobial activity via membrane disruption
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98
Q

What is the body’s only means of eliminating cholesterol?

A

bile formation

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99
Q

Describe bilirubin metabolism.

A
  • protoporphyrin is reduced to unconjugated bilirubin
  • water-insoluble UCB is transported to the liver via albumin where it is conjugated with glucuronate by uridine glucuronyl transferase (UGT) in hepatocytes
  • CB is water soluble and excreted in bile
  • in the bile gut bacteria metabolize CB to urobilinogen
  • most urobilinogen is oxidized and excreted in the feces as stercobilin, giving stool it’s brown color
  • some urobilinogen enters enterohepatic circulation and is reabsorbed
  • the rest is excreted in urine as urobilin, giving it a yellow color
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100
Q

Cleft lips and palates result from failure of what process?

A

failure of the facial prominences to grow and fuse together

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101
Q

How many facial prominences are there?

A

five: 1 superior, 2 lateral, 2 inferior

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102
Q

Aphthous Ulcer

A
  • a painful, superficial ulceration of the oral mucosa
  • typically arises during periods of stress and will resolve spontaneously
  • characterized by a grayish base (granulation tissue) surrounded by erythema
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103
Q

Behcet Syndrome

A

an immune complex-mediated small-vessel vasculitis that leads to a syndrome of recurrent aphthous ulcers, genital ulcers, and uveitis

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104
Q

Oral Herpes

A
  • vesicles involving the oral mucosa that rupture, resulting in shallow, painful, red ulcers
  • most cases are due to HSV-1 infection
  • primary infection occurs in childhood but virus remains dormant in the ganglia of the trigeminal nerve
  • often reactivated by stress or sunlight
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105
Q

Squamous Cell Carcinoma of the Mouth

A
  • a malignant neoplasms of squamous cells lining the oral mucosa
  • most often arisen in the floor of the mouth
  • risk factors include tobacco and alcohol
  • oral leukoplakia and erythroplakia (vascularized leukoplakia) can be precursor lesions, but erythroplakia is more suggestive of dysplasia than leukoplakia
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106
Q

What is luekoplakia? What can it be confused with?

A
  • it is an oral lesion described as a white plaque that cannot be scraped away
  • often represents squamous cell dysplasia and in those cases it is a precursor lesion to squamous cell carcinoma of the oral mucosa
  • may be confused with oral candidiasis or hairy leukoplakia; however, oral candidiasis is usually easily scraped away and hairy leukoplakia (a form of hyperplasia induced by EBV) arises mostly on the lateral tongue with a shaggy appearance
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107
Q

Hairy Leukoplakia

A
  • hyperplasia of the oral mucosa caused by EBV in immunocompromised patients
  • takes the form of a white, shaggy lesion on the lateral tongue
  • not to be confused with leukoplakia or oral candidiasis
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108
Q

Oral Candidiasis v. Leukoplakia v. Hairy Leukoplakia

A
  • oral candidiasis is a fungal infection of the mouth seen in those who are immunocompromised, and it takes the from of easily scraped away white lesions
  • leukoplakia is a white lesion that cannot be scraped away, and it often represents dysplasia in which case it is a precursor lesion to squamous cell carcinoma of the oral mucosa
  • hairy leukoplakia is an EBV-induced hyperplasia that takes the form of a shaggy white lesion on the lateral tongue in immunocompromised individuals
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109
Q

Which is more suggestive of squamous cell carcinoma of the oral mucosa, leukoplakia or erythroplakia?

A

erythroplakia is vascularized leukoplakia and thus more likely to be malignant

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110
Q

What are the three major salivary glands?

A
  • parotid
  • submandibular
  • sublingual
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111
Q

Mumps

A
  • an infection with mumps virus
  • results in bilateral inflammation of the parotid salivary glands
  • complications include orchitis, pancreatitis, and aseptic meningitis
  • orchitis carries a risk of sterility but is only likely in those over the age of 10 who contract mumps
  • serum amylase is increased due to salivary or pancreatic involvement
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112
Q

Sialadenitis

A
  • inflammation of the salivary gland

- most commonly caused by an obstructing stone, leading to a unilateral S. aureus infection

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113
Q

What is the most common tumor and the most common malignancy of the salivary gland?

A
  • tumor: pleomorphic adenoma

- malignancy: mucoepidermoid carcinoma

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114
Q

Pleomorphic Adenoma

A
  • the most common benign tumor of the salivary gland
  • it is composed of stromal tissue and epithelial tissue (i.e. pleomorphic)
  • it most often affects the parotid and presents as a mobile, painless, circumscribed mass at the angle of the jaw
  • has a high rate of recurrence due to it’s irregular borders and often incomplete resection
  • rarely, may transform into carcinoma, which often presents with signs of facial nerve damage after many recurrences of the benign tumor
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115
Q

A patient presents with recurrent pleomorphic adenoma that has begun to cause facial nerve problems. What has likely occurred?

A
  • recurrent pleomorphic adenoma has become malignant

- as such it has become invasive and has affected the facial nerve running through the parotid

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116
Q

What nerve runs through the parotid gland?

A

the facial nerve

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117
Q

Warthin Tumor

A
  • a benign cystic tumor of the salivary gland
  • with abundant lymphocytes and germinal centers (i.e. cystic tumor with lymph node tissue)
  • almost always affects the parotid
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118
Q

Which salivary gland is most affected by pathology?

A

the parotid

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119
Q

Mucoepidermoid Carcinoma

A
  • the most common malignancy of the salivary gland
  • composed of mutinous and squamous cells
  • usually affects the parotid and commonly involves the facial nerve
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120
Q

Esophageal Web

A
  • a thin protrusion of the esophageal mucosa into the lumen, most often seen in the upper esophagus
  • presents with dysphagia for poorly chewed food
  • increases the risk for esophageal squamous cell carcinoma
  • a feature of Plummer-Vinson syndrome (iron deficiency anemia, esophageal web, and beefy-red tongue due to atrophic glossitis)
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121
Q

What are the features of Plummer-Vinson syndrome?

A
  • iron deficiency anemia
  • esophageal web
  • beefy-red tongue due to atrophic glossitis
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122
Q

Mallory-Weiss Syndrome

A
  • a longitudinal laceration of the mucosa at the gastroesophageal junction caused by severe vomiting
  • most often seen in alcoholics and bulimics
  • presents with painful hematemsis
  • risk of Boerhaave syndrome with rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema
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123
Q

Wha tis Boerhaave syndrome?

A

rupture of the esophagus, which leads to air in the mediastinum and in subcutaneous tissue, which can be heard as crackling when pressing down on the skin

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124
Q

Esophageal Varices

A
  • dilated submucosal veins in the lower esophagus
  • arises secondary to portal hypertension because blood can no longer flow into the left gastric vein and then the portal vein
  • typically asymptomatic but may present with a painless hematemesis
  • risk of rupture, which is the most common cause of death in those with cirrhosis
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125
Q

Where along the length of the esophagus are varices most likely?

A

in the lower third

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126
Q

What is the most common cause of death in those with cirrhosis?

A

rupture of esophageal varices

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127
Q

Achalasia

A
  • disordered esophageal motility with an inability to relax the LES
  • caused by damage to ganglion cells in the myenteric plexus, which are important for motility
  • presents with dysphagia for both solids and liquids, putrid breath, high LES pressure, and “bird beak” sign due to dilation of the esophagus
  • have an increased risk for esophageal squamous cell carcinoma
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128
Q

GERD

A
  • reflux of acid from the stomach due to reduced LES tone
  • risk factors include alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal hernia
  • presents with heartburn, adult-onset asthma and cough, damage to enamel of teeth, and ulceration with stricture (ulcer heals by fibrosis, which constricts)
  • risk of Barrett esophagus as a late complication
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129
Q

Barrett Esophagus

A
  • a metaplasia of the lower esophageal mucosa from stratified squamous to conciliated columnar with goblet cells
  • may progress to dysplasia and adenocarcinoma
130
Q

Esophageal Carcinoma

A
  • either adenocarcinoma (more common in the West) or squamous cell carcinoma (more common worldwide)
  • adenocarcinoma refers to a proliferation of glands, and arises from pre-existing Barrett esophagus in the lower third of the esophagus
  • squamous cell carcinoma arises in the upper and middle thirds of the esophagus in response to irritation; risk factors include alcohol, tobacco, very hot tea, achalasia, esophageal web, and esophageal injury
  • both present late and thus have a poor prognosis
  • symptoms include progressive dysphagia (solids then liquids), weight loss, pain, and hematemesis
  • squamous cell often presents with hoarse voice and cough as well due to involvement of the recurrent laryngeal nerve and trachea, respectively
  • spreads to the cervical, mediastinal and tracheobronchial, or celiac and gastric lymph nodes depending on if it is in the upper, middle, or lower portion of the esophagus
131
Q

Where does esophageal carcinoma spread?

A
  • upper ⅓: cervical nodes
  • middle ⅓: mediastinal or tracheobronchial nodes
  • lower ⅓: celiac or gastric nodes
132
Q

Acute Gastritis

A
  • acidic damage to the stomach mucosa due to an imbalance between acidity and mucosal defenses
  • risk factors include: severe burn (hypovolemia leads to decreased blood supply), NSAIDs (reduced prostaglandin production), heavy alcohol consumption, chemotherapy, increased intracranial pressure (stimulates vagus leading to acid production), and shock (reduced blood flow)
  • the result is superficial inflammation, erosion, or ulcer
133
Q

What defenses protect the gastric mucosa from gastric acid?

A
  • a mucin layer produced by foveolar cells
  • bicarbonate secreted by surface epithelium
  • normal blood supply, which provides necessary nutrients and carries away any acid that does happen to get through the other defenses
  • prostaglandins, which inhibit acid production and stimulate mucin/bicarbonate secretion plus blood flow
134
Q

What is a Curling ulcer?

A

a stomach ulcer that results after a severe burn, because burn injuries lead to hypovolemia and adequate blood supply is an important defense for the gastric mucosa against gastric acid

135
Q

What is a Cushing ulcer?

A

a stomach ulcer that results from increased ICP, which stimulates the vagus nerve and promotes increased gastric acid production

136
Q

Why are NSAIDs likely to cause ulcers?

A

because they reduce prostaglandin formation and PGs are needed to maintain blood flow to the gastric mucosa in addition to promoting bicarbonate and mucin secretion

137
Q

What is the difference between a gastric erosion and gastric ulcer?

A

an erosion is a loss of superficial epithelium while an ulcer is a loss of the mucosal layer

138
Q

Chronic Gastritis

A
  • chronic inflammation of the stomach mucas
  • classified as either chronic autoimmune gastritis or chronic H. pylori gastritis (more common)
  • chronic autoimmune gastritis targets gastric parietal cells located in the body and fundus while H. pylori preferentially affects the antrum
139
Q

Chronic Autoimmune Gastritis

A
  • a form of chronic gastritis due to autoimmune destruction of gastric parietal cells in the stomach body and fundus
  • antibodies against parietal cells and/or intrinsic factor are diagnostic but pathogenesis is mediated by T cells
  • presents with atrophy of the mucosa with intestinal metaplasia (lots of goblet cells), achlorhydria with increased gastrin levels and antral G-cell hyperplasia, and pernicious anemia
  • increased risk for intestinal type gastric adenocarcinoma
140
Q

Chronic H. pylori Gastritis

A
  • a form of chronic gastritis due to H. pylori induced inflammation
  • more common than chronic autoimmune gastritis
  • H. pylori ureases and proteases weaken mucosal defenses, particularly in the antrum, and contribute to mucosal inflammation
  • presents with epigastric abdominal pain
  • increases risk for ulceration, intestinal type gastric adenocarcinoma, and MALT lymphoma
  • treat with triply therapy (PPI, amoxicillin/metronidazole, and clarithromycin)
  • confirm eradiaction with negative urea breath test and lack of stool antigen
  • treatment resolves ulcers and reverses intestinal metaplasia
141
Q

Duodenal Ulcer

A
  • a solitary mucosal ulcer
  • more common than a gastric ulcer
  • most cases are due to H. pylori but a few are due to a gastrinoma (ZE syndrome)
  • presents with epigastric pain that improves with meals since the duodenum preps for the meal by increasing protective measures
  • diagnose using endoscopic biopsy, which shows hypertrophy of Brunner glands
  • anterior wall is more commonly affected but in the posterior duodenal, rupture is more likely
  • rupture leads to hemorrhage of the gastroduodenal artery or acute pancreatitis and you may see free air under the diaphragm with referred pain to the shoulder via the phrenic nerve
  • almost never malignant (in contrast to gastric ulcers)
142
Q

Rupture of a duodenal ulcer is most likely when it is located where? What are the likely complications?

A
  • rupture most likely in the posterior wall of the proximal duodenum
  • complications include hemorrhage of the gastroduodenal artery or acute pancreatitis
143
Q

Gastric Ulcer

A
  • a solitary mucosal ulcer, most often in the lesser curvature of the antrum
  • less common than a duodenal ulcer
  • usually due to H. pylori but may also be caused by use of NSAIDs or bile reflux
  • presents with epigastric pain that worsens with meals because acid production increases
  • rupture carries a risk of bleeding from the left gastric artery
  • can be caused by intestinal type gastric carcinoma, in which was they tend to be larger and irregular with heaped up margins
144
Q

How does a duodenal ulcer compare to a gastric ulcer?

A
  • duodenal are more common
  • duodenal are more often caused by H. pylori
  • both present with epigastric pain but that associated with duodenal ulcers gets better with meals and that associated with gastric ulcers get worse with meals
  • rupture of a duodenal ulcer is likely to cause bleeding of the gastroduodenal artery while rupture of a gastric ulcer is likely to cause bleeding of the left gastric artery
  • duodenal ulcers are almost never malignant but gastric ulcers can be caused by intestinal type gastric carcinoma
145
Q

How can a malignant gastric ulcer be differentiated from a benign one during endoscopy?

A
  • benign ones tend to be smaller (< 3 cm) and sharply demarcated
  • malignant ones tend to be larger, irregular, and surrounded by heaped up margins
146
Q

What are the two types of gastric carcinoma?

A

intestinal and diffuse

147
Q

Intestinal Type Gastric Carcinoma

A
  • an adenocarcinoma
  • presents as a large, irregular ulcer with heaped up margins, most often in the lesser curvature of the antrum
  • risk factors include intestinal metaplasia (with goblet cells) due to chronic gastritis, nitrosamines in smoked foods, and type A blood group
  • symptoms arise late with weight loss, abdominal pain, anemia, and early satiety
  • may present with acanthosis nigricans or Leser-Trelat sign
  • spread is to the left supraclavicular node known as Virchow’s node
  • most likely to metastasize to the liver but may metastasize to the periumbilical region, known as a Sister Mary Joseph nodule
148
Q

Diffuse Type Gastric Carcinoma

A
  • an adenocarcinoma
  • characterized by signet ring cells that diffusely infiltrate the gastric wall along with desmoplasia that results in thickening of the stomach wall known as linitis plastica
  • not associated with H. pylori, intestinal metaplasia, or nitrosamines
  • symptoms arise late and include weight loss, abdominal pain, anemia, and early satiety
  • may present with acanthosis nigricans or Leser-Trelat sign
  • spread is to the left supraclavicular node known as Virchow’s node
  • most likely to metastasize to the liver but may metastasize to the ovaries bilaterally, which is known as a Krukenburg tumor
149
Q

What are signet cells indicative of?

A

diffuse gastric carcinoma, which may have spread to the liver or bilaterally to the ovaries where it is known as a Krukenburg tumor

150
Q

What is Virchow’s node?

A

the left supraclavicular node where gastric carcinoma is most likely to spread to

151
Q

What is Leser-Trelat sign?

A

the outbreak of many seborrheic keratoses on the skin, often indicating internal malignancy

152
Q

Meckel Diverticulum

A
  • the most common congenital anomaly of the GI tract
  • a true diverticulum (outpouching of all three layers of the bowel wall)
  • arising from failure fate vitelline duct to fully involute
  • follows the “rule of 2s”: seen in 2% of the population, 2 inches long, located in the small bowel with 2 feet of the ileocecal valve, presenting in the fist 2 years of life with bleeding, volvulus, intussusception, or obstruction (mimics appendicitis), 2 times as likely in males, possibility for 2 types of epithelia (gastric/pancreatic)
  • bleeding is due to heterotopic gastric mucosa
  • however, most often asymptomatic
  • diagnosed via a pertechnetate study for uptake by ectopic gastric mucosa
153
Q

If an adult presents with new-onset asthma, what should you consider as a possible cause?

A

GERD

154
Q

If the vitelline duct fails to involute at all, what is the most obvious sign after birth?

A

passing of meconium by the umbilicus

155
Q

Volvulus

A
  • a twisting of the bowel along it’s mesentery
  • resulting in obstruction of the bowel and disruption of the blood supply with infarction
  • most common in the sigmoid colon of the elderly or the cecum if the patient is a younger adult since these are areas with superfluous mesentery
  • presents with abdominal pain and red “currant jelly” stool
156
Q

Intussusception

A
  • a telescoping of the proximal segment of bowel forward into the distal segment caused by peristalsis pulling a “leading edge” forward
  • leading edge refers to the focus of traction and in children this is most often lymphoid hyperplasia arising in the terminal ileum with intussusception into the cecum or a Meckel diverticulum
  • in adults, the leading edge is more commonly formed by a tumor
  • the deformation results in obstruction and disruption of the blood supply with infarction
  • can be seen as a “bull’s eye appearance on ultrasound
  • presents with abdominal pain and “currant jelly” stools
157
Q

Why is the small bowel so susceptible to infarction?

A

because it requires lots of ATP, and therefore oxygen, for absorption of nutrients

158
Q

Small Bowel Infarction

A
  • common because of the high energy needs of the small bowel
  • simple hypotension is likely to cause a mucosal infarction while transmural infarction occurs with thrombosis of the SMA or mesenteric vein
  • presents with abdominal pain, bloody diarrhea, and decreased bowel sounds
159
Q

Where is lactase?

A

it is found in the brush border of enterocytes

160
Q

Lactase catalyzes what reaction?

A

lactose to glucose and galactose

161
Q

What can cause lactose intolerance?

A
  • may be congenital due to an AR disorder
  • acquired, developing in late childhood
  • or transient after a small bowel infection since lactase is highly susceptible to injury
162
Q

Celiac Disease

A
  • an immune mediated damage of the small bowel villi due to gluten exposure, and in particular the component gliadin
  • strongly associated with HLA-DQ2 and HLA-DQ8
  • damage is mediated by CD4 cells
  • presents in children with abdominal distention, diarrhea, and failure to thrive or in adults with chronic diarrhea and bloating
  • small, herpes-like vesicles may arise on the skin, known as dermatitis herpetiformis, due to IgA deposition at the tips of dermal papillae
  • associated with IgA deficiency but labs find IgA or IgG against endomysium, tTG, or gliadin
  • biopsy reveals flattened villi, hyperplasia of crypts, and increased intraepithelial lymphocytes in the duodenum
  • small bowel carcinoma and T-cell lymphoma are late complications that often presents as refractory disease despite good dietary control
163
Q

Describe gluten metabolism as it relates to Celiac disease.

A
  • gluten is absorbed
  • gliadin is deaminated by tissue transflutaminase (tTG)
  • this is presented via MHC-II and activates helper T cells
164
Q

Patients with Celiac disease who appear to have excellent dietary control but continue to experience symptoms likely have what occurring?

A

they likely have either a small bowel carcinoma or T-cell lymphoma

165
Q

Tropical Sprue

A
  • damage to small bowel villi due to an unknown organism found in tropical regions, causing malabsorption
  • arises after infectious diarrhea and responds to antibiotics
  • damage is most prominent in the jejunum and ileum
166
Q

Describe dietary fat digestion and absorption.

A
  • broken down by pancreatic lipases
  • bile helps emulsify the metabolites into small droplets, called micelles
  • micelles diffuse into enterocytes and are repackaged into chylomicrons
  • chylomicrons are too big to enter the blood stream directly, so they are exported into the lamina propria
  • there they are absorbed into lymphatic spaces called lacteals, which transport them eventually into the blood
167
Q

Whipple Disease

A
  • systemic tissue damaged characterized by macrophages loaded with partially destroyed Tropheryma whippelii in lysosomes
  • most often affects the small bowel propria in which case macrophages compress lacteals, preventing the absorption of chylomicrons and contributing to fat malabsorption and steatorrhea
  • may also affect the synovium of joints, cardiac valves, lymph nodes, or CNS
  • organism is intracellular gram positive and stains PAS positive in foamy macrophages
168
Q

Abetalipoproteinemia

A
  • an autosomal recessive deficiency of B-48 or B-100
  • B-48 deficiency causes malabsorption as it is required for chylomicron formation
  • B-100 causes an absence of plasma VLDL and LDL as it is required for their formation
169
Q

Carcinoid Tumor

A
  • a malignant proliferation of neuroendocrine cells, which often secrete serotonin
  • can arise anywhere along the gut but the small bowel is most common where they grow as submucosal polyp-like nodules
  • secreted serotonin is metabolized by liver MAO into 5-HIAA, so they are asymptomatic until they metastasize to the liver
  • once metastasized they produce carcinoid syndrome and carcinoid heart disease
  • contain neurosecretory granules and are thus chromogranin positive; 5-HIAA levels are elevated in urine
170
Q

What are the features of carcinoid syndrome?

A
  • bronchospasm, diarrhea, and flushing of the skin

- often precipitated by alcohol or emotional stress, which stimulate serotonin release from the tumor

171
Q

What are the features of carcinoid heart disease?

A
  • right-sided valvular fibrosis leading to tricupsid regurgitation and pulmonary valve stenosis
  • left-sided valvular lesions not seen due to MOA in the lung, which metabolizes the serotonin that causes carcinoid heart disease
172
Q

Acute Appendicitis

A
  • the most common cause of acute abdomen
  • caused by obstruction of the appendix, most commonly by lymphoid hyperplasia in children or a fecalith in adults
  • presents with periumbilical pain that migrates and eventually localizes to the right lower quadrant over McBurney’s point
  • rupture will result in peritonitis with guarding and rebound tenderness
  • may be complicated by a periappendiceal abscess
173
Q

Inflammatory Bowel Disease

A
  • a chronic, relapsing inflammation of the bowel
  • thought to be mediated by an abnormal immune response to enteric flora
  • most common in young women
  • subclassified as either ulcerative colitis or Crohn disease
174
Q

Ulcerative Colitis

A
  • a form of inflammatory bowel disease mediated by Th2 cells
  • affects the mucosal and submucosa only, forming ulcers
  • begins in the rectum and extends proximally in a continuous manner, limited to the colon
  • presents with left lower quadrant pain and blood diarrhea
  • grossly, there are pseudopolyps and a loss of haustra, known as the “lead pipe” sign
  • histology reveals crypt abscesses with neutrophils
  • complications include toxic megacolon and carcinoma; importantly the risk of carcinoma is based on extent of colon involved and duration of disease (rarely before 10 years)
  • may present with primary sclerosing cholangitis or the presence of p-ANCA
  • smoking is protective
  • treated with 5-aminosalicylic preparations, 6-MP, infliximab, or colectomy
175
Q

Crohn Disease

A
  • a form of inflammatory bowel disease mediated by Th1
  • affects the full thickness of the wall, forming knife-like fissures
  • can affect anywhere in the GI tract with skip lesions, but the terminal ileum is most common and colon is least
  • presents with right lower quadrant pain and non-blood diarrhea in contrast to UC
  • grossly, there is cobblestoning of the mucosa, creeping fat, and stricture as healing involves myofibroblasts
  • histology reveals granulomas and lymphoid aggregates
  • complications include malabsorption, calcium oxalate nephrolithiasis, fistula formation, strictures/obstruction, and carcinoma if the colon is involved
  • may present with arthritis, uveitis, or erythema nodosum
  • smoking is not protective
  • treated with corticosteroids, azathioprine, antibiotics, infliximab, or adalimumab
176
Q

Hirschsprung Disease

A
  • defective relaxation and peristalsis of the rectum and distal sigmoid colon
  • due to a congenital failure of ganglion cells (neural crest derived) to descend into the myenteric and submucosal plexuses
  • strongly associated with Down syndrome and RET mutations
  • clinical features are based on obstruction and include failure to pass meconium, an empty rectal vault of digital exam, megacolon, and bilious emesis
  • requires a rectal SUCTION biopsy to sample the two plexuses, which aren’t biopsied normally
  • treatment involves resection of the involved bowel
177
Q

What is the function of the myenteric and submucosal plexuses of the GI tract?

A
  • the myenteric is located between the inner circular and outer longitudinal muscle layers of the muscularis propria and regulates motility
  • the submucosal plexus is located in the submucosa and regulates blood flow, secretions, and absorption
178
Q

Colonic Diverticula

A
  • an out pouching of mucosa and submucosa only through the muscularis propria (false diverticulum)
  • risk factors are those that are related to wall stress: constipation, straining, low-fiber diet, and age
  • they arise where the vase recta transverse the muscularis propria because this is a weak point in the wall
  • the sigmoid colon is most often affected
  • usually asymptomatic but may cause hematochozia, diverticulitis, or fistula
179
Q

Diverticulitis

A
  • a diverticulosis with inflamed micro perforations
  • classically presenting with LLQ pain, fever, and leukocytosis, mimicking appendicitis but on the left
  • complications include abscess, fistula, obstruction, or perforation
  • treat with antibiotics and complications with percutaneous drainage or surgery
180
Q

How does colovesicular fistula present?

A
  • presents with air or stool in the urine

- often due to rupture of a diverticula

181
Q

Angiodysplasia

A
  • an acquired malformation of mucosal and submucosal capillary beds
  • usually arises in the cecum and right colon due to high wall tension
  • classically presents as hematochezia in older adults
182
Q

How are colonic diverticula and angiodysplasia related?

A
  • both are due to wall stress and present most often in the elderly with hematochezia
  • however, diverticula typically occur on the left side in the sigmoid colon and angiodysplasia occur on the right side in the cecum and ascending colon
183
Q

Hereditary Hemorrhagic Telangiectasia

A
  • an autosomal dominant disorder that results in thin-walled blood vessels, particularly in the mouth and GI tract
  • rupture presents as bleeding/petechiae
184
Q

Ischemic Colitis

A
  • ischemic damage to the colon, most often at the splenic flexure, which is a watershed area of the SMA
  • most often due to atherosclerosis of the SMA
  • presents with post-prandial pain (because that is when energy requirement is the highest) and weight loss
  • if it progresses to infarction, it presents with pain and bloody diarrhea
185
Q

Irritable Bowel Syndrome

A
  • a relapsing abdominal pain with bloating, flatulence, and change in bowel habits that improves with defecation
  • most often seen in middle-aged females
  • related to disturbed intestinal motility but there are no identifiable pathologic changes
  • increased fiber may improve symptoms
186
Q

What are the two most common types of colonic polyps?

A

hyperplastic and adenomatous

187
Q

Hyperplastic Colonic Polyps

A
  • the most common type of colonic polyp
  • they form due to hyperplasia of glands
  • have a “serrated” appearance on microscopy
  • they have no malignant potential
188
Q

Adenomatous Colonic Polyps

A
  • a neoplastic proliferation of glands
  • benign but premalignant and may progress to adenocarcinoma via the adenoma-carcinoma sequence
  • most likely to progress to carcinoma are those more than 2 cm in size, with sessile growth (not pedunculate), and villous histology
  • goal of a colonoscopy is to remove all adenomatous polyps
189
Q

What is the adenoma-carcinoma sequence?

A
  • a molecular sequence by which normal colonic mucosa forms adenomatous polyps and then carcinoma
  • begins with a double KO of the tumor suppressor gene APC, which increases the risk for polyp formation
  • a K-ras mutation then induces polyp formation
  • p53 mutation and increased expression of COX then allows for progression to carinoma
190
Q

What OTC medication impedes the adenoma-carcinoma sequence? How?

A

aspirin impedes progression because it limits COX expression, which is an important last step between adenomatous polyp and carcinoma

191
Q

How do we screen for colon cancer?

A
  • colonoscopy

- testing for fecal occult blood

192
Q

What is the goal of colonoscopy?

A

to remove adenomatous polyps before they progress

193
Q

Which polyps are removed on a colonoscopy?

A

all polyps are removed because hyper plastic and adenomatous polyps look identical on colonoscopy

194
Q

Which adenomatous polyps have the greatest risk for progression to carcinoma?

A

those more than 2 cm, with sessile growth (not pedunculate), or villous histology

195
Q

Familial Adenomatous Polyposis

A
  • an autosomal dominant disorder characterized by 100s or 1000s of adenomatous colonic polyps
  • due to an inherited APC mutation on chromosome 5 (a tumor suppressor gene involve in the adenoma-carcinoma sequence)
  • colon and rectum are removed prophylactically; otherwise, almost all patients develop carcinoma by age 40
  • associated with CRC on the left-side of the colon
  • Gardner syndrome is a subpopulation of FAP with fibrzomatosis and osteomas
  • Turcot syndrome is a subpopulation of FAP with CNs tumors
196
Q

Turcot Syndrome

A

a syndrome of familial adenomatous polyposis (APC mutation) and CNS tumors like medulloblastoma and glial tumors

197
Q

Gardner Syndrome

A

a syndrome including familial adenomatous polyposis (APC mutation), fibromatosis, and osteoma

  • fibromatosis is a non-neoplastic proliferation of fibroblasts in the retroperitoneum, which destroys local tissue
  • additional findings include congenital hypertrophy of teh retinal pigment epithelium and impacted/supernumeray teeth
198
Q

Juvenile Polyp

A
  • a sporadic, hamartomatous, benign polyp that arises in children
  • tends to prolapse and bleed
  • juvenile polyposis is characterized by multiple in the stomach and colon
  • tend to increase the risk for carcinoma
199
Q

Peutz-Jeghers Syndrome

A
  • an autosomal dominant syndrome of multiple hamartomatous, benign polyps throughout the GI tract with hyperpigmentation of the lips, oral mucosa, and genital skin
  • increases the risk for colorectal, breast, and gynecologic cancer
200
Q

Colorectal Carcinoma

A
  • the third most common site of cancer and third most common cause of cancer-related death
  • adenoma-carcinoma sequence tends to be at work in cancer on the left and microsatellite instability on the right
  • left-sided carcinoma tends to grow as a napkin-ring lesion with decreased stool caliber, blood-streaked stools, and left lower quadrant pain
  • right-sided usually grow as a raised lesion with iron-deficiency anemia and vague pain
  • increases the risk for S. bovis endocarditis
  • CEA is an important tumor marker, useful for assessing treatment response and detecting recurrence but not for screening
  • typically don’t spread until they’ve invaded more than the mucosa because the mucosa lacks lymphatics
  • most commonly spreads to the liver
201
Q

When does screening for colorectal carcinoma begin?

A

age fifty

202
Q

What is microsatellite instability?

A
  • a molecular pathway for colorectal cancer
  • micro satellites are repeating sequences of noncoding DNA that tend to remain unchanged during cell division
  • instability is indicative of a defective DNA copy mechanism, which contributes to the formation of cancer
  • most often associated with right-sided colorectal cancer
203
Q

Hereditary Nonpolyposis Colorectal Carcinoma

A
  • aka Lynch syndrome, the typical example of microsatellite instability
  • an inherited mutation in a DNA mismatch repair enzyme increases the risk for colorectal, ovarian, and endometrial carcinoma
  • in such cases, colorectal carcinoma tends to arise de novo rather than from an adenomatous polyp and at a relatively early age on the right-side
204
Q

Acute Pancreatitis

A
  • inflammation and hemorrhage of the pancreas due to premature activation of trypsin and autodigestion
  • results in liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the surrounding peripancreatic fat
  • most commonly due to (“I GET SMASH”): idiopathic, gallstones, ethanol, trauma, scorpion stings, mumps/malignancy, autoimmune, steroids, hyperlipidemia/hypercalcemia or rupture of a posterior duodenal ulcer
  • presents with n/v and epigastric pain radiating to the back
  • serum lipase and amylase are both elevated, but lipase is more specific
  • hypocalcemia results from saponification in fat necrosis
  • complications include shock, pancreatic pseudocyst, pancreatic abscess formation, or DIC/ARDS (enzymes enter blood)
205
Q

Pancreatitis results in what sort of necrosis?

A
  • liquefactive hemorrhagic necrosis of the parenchyma

- fat necrosis of the surrounding peripancreatic fat

206
Q

What is a pancreatic pseudocyst?

A
  • a complication of acute pancreatitis
  • fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes
  • presents with an abdominal mass and persistently elevated serum amylase even after pancreatitis has been dealt with
  • rupture is associated with enzyme release and hemorrhage
207
Q

What are two reasons amylase may remain elevated after treating someone with pancreatitis?

A
  • a pancreatic pseudocyst

- a pancreatic abscess

208
Q

Chronic Pancreatitis

A
  • fibrosis of the pancreatic parenchyma secondary to recurrent acute pancreatitis
  • most often seen in alcoholics and those with cystic fibrosis
  • presents with epigastric abdominal pain that radiates to the back, pancreatic insufficiency resulting in malabsorption with steatorrhea and fat-soluble vitamin deficiencies, and secondary diabetes mellitus
  • dystrophic calcification can be seen on imaging
  • poses a risk for pancreatic carcinoma
209
Q

Epigastric pain that radiates to the back indicates what?

A

pancreatitis

210
Q

Pancreatic Adenocarcinoma

A
  • an adenocarcinoma arising from the pancreatic ducts rather than the acini
  • risk factors include smoking and chronic pancreatitis
  • presents with epigastric abdominal pain, weight loss, obstructive jaundice with pale stools and palpable gall bladder (when arising in the head of the pancreas), secondary diabetes mellitus (when arising in the body or tail), pancreatitis and migratory thrombophlebitis
  • serum marker is CA19-9
  • treatment is a Whipple procedure but the prognosis is very poor
211
Q

What serum marker is indicative of pancreatic carcinoma?

A

CA 19-9

212
Q

What happens in a Whipple procedure?

A

the head and neck of the pancreas, proximal duodenum, and gallbladder are removed

213
Q

How does pancreatic carcinoma in the head/neck differ from that arising in the body/tail?

A
  • in the head, you’re more likely to have obstructive jaundice with pale stools and a palpable gallbladder
  • in the tail, you’re more likely to have very late secondary diabetes without obesity
214
Q

A 70-year old, thin women presents with new-onset secondary diabetes. What might you consider as a diagnosis?

A

pancreatic carcinoma in the tail/body of the pancreas

215
Q

What is migratory thrombophlebitis?

A

swelling, erythema, and tenderness in the extremities, sometimes seen in those with pancreatic carcinoma

216
Q

Biliary Atresia

A
  • failure to form or early destruction of the extra hepatic biliary tree
  • leads to biliary obstruction within the first two months of life, which presents with jaundice and progresses to cirrhosis
217
Q

What are the two major kinds of gall stones? Which is more common?

A

cholesterol stones are more common than bilirubin ones

218
Q

What three changes with lead to precipitation of cholesterol or bilirubin and formation of a cholelithiasis?

A
  • supersaturation
  • decreased phospholipids or bile acids which normally serve to increase solubility
  • stasis, which allows for growth of bacteria which deconjugate bile
219
Q

What is a common drug that induces cholelithiasis?

A

cholestyramine because it binds bile and inhibits reabsorption, reducing the bile content of the gallbladder, reducing solubility of cholesterol and bilirubin

220
Q

Why does stasis contribute to the formation of a cholelithiasis?

A
  • the normal flow of bile clears the biliary tree of bacteria
  • during times of stasis, bacteria are able to ascend grow
  • they are capable of deconjugating bilirubin, which makes it insoluble
221
Q

Cholesterol Stones

A
  • the most common type of gallstone
  • usually radiolucent and yellow on gross exam
  • risk factors include age, greater exposure to estrogen, clofibrate, Native American ethnicity, Crohn disease, and cirrhosis
  • usually asymptomatic but may lead to biliary colic, acute or chronic cholecystitis, ascending cholangitis, gallstone ileum, or gallbladder cancer
222
Q

Why is estrogen a risk factor for cholesterol gallstones?

A

because it increases the activity of HMG-CoA reductase, promoting cholesterol synthesis while also increasing lipoprotein receptor expression by hepatocytes, increasing their cholesterol uptake

223
Q

Why does Crohn disease contribute to the formation of gallstones?

A

because it can damage the ileum and impair recycling of bile salts and acids, reducing the solubility of cholesterol in the gall bladder

224
Q

Bilirubin Cholelithiasis

A
  • a radiopaque, pigmented gallstone
  • risk factors include extravascular hemolysis, which increases bilirubin content in the bile and biliary tract infection (E. coli, A. lumbricoides, or Clonorchis sinensis)
  • usually asymptomatic but may lead to biliary colic, acute or chronic cholecystitis, ascending cholangitis, gallstone ileum, or gallbladder cancer
225
Q

Ascaris lumbricoides

A
  • a common roundworm
  • common in areas with poor sanitation because it utilizes fecal-oral transmission
  • infects the biliary tract and increases the risk for gallstones
226
Q

Clonorchis sinensis

A
  • a liver fluke endemic to China, Korea, and Vietnam

- infects the biliary tract and increases the risk for gallstones, cholangitis, and cholangiocarcinoma

227
Q

Biliary Colic

A
  • a waxing and waning right upper quadrant pain due to gallbladder contracting against a stone lodged in the duct
  • relieved by passaged of the stone
  • may cause acute pancreatitis or obstructive jaundice if it is lodged in the common bile duct
228
Q

Acute Cholecystitis

A
  • acute inflammation of the gallbladder wall
  • often due to an impacted stone in the cystic duct which causes dilatation with pressure ischemia, bacterial overgrowth (commonly E. coli), and inflammation
  • presents with right upper quadrant pain radiating to the scapula, a high WBC count, n/v, and elevated serum alkaline phosphatase
  • Murphy sign is likely positive (respiratory arrest on palpation)
  • risk of rupture if untreated
229
Q

What causes right upper quadrant pain that radiates to the scapula?

A

acute cholecystitis

230
Q

Chronic Cholecystitis

A
  • chronic inflammation of the gallbladder
  • most often due to chemical irritation from longstanding cholelithiasis
  • characterized by herniation of the gallbladder mucosa into the muscular wall, forming a Rokitansky-Aschoff sinus
  • presents with vague right upper quadrant pain, especially after eating
  • porcelain gallbladder is a late complication described as a shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification, which increases the risk for carcinoma
  • treat with cholecystectomy
231
Q

What is porcelain gallbladder?

A

a late complication of chronic cholecystitis described as a shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification, which increases the risk for carcinoma

232
Q

Ascending Cholangitis

A
  • a bacterial infection of the bile ducts
  • most often due to an ascending infection with enteric gram-negative bacteria
  • presents as sepsis with jaundice and abdominal pain
  • increased incidence with choledocholithiasis (presence of a stone in the duct), which reduces bile flow
233
Q

Gallstone Ileus

A

a phenomenon whereby gallstones enter and obstruct the small bowel by way of a fistula formed during a bout of cholecystitis with rupture

234
Q

Gallbladder Carcinoma

A
  • an adenocarcinoma arising from the wall
  • major risk factor is gallstones, especially when complicated by porcelain gallbladder
  • classically presents as cholecystitis in an elderly woman
235
Q

What is jaundice due to?

A

an elevated serum bilirubin caused by a disturbance in normal bilirubin metabolism

236
Q

How does extravascular hemolysis cause jaundice? How does this manifest compared to other causes of jaundice?

A
  • it results in high levels of UCB, which overwhelm the conjugating ability to the liver
  • as a result there is increased UCB in the blood
  • the conjugating ability is maxed out, so there is also more CB in the bile than usual; this manifests as dark urine and a risk for bilirubin gallstones
237
Q

Physiologic Jaundice of the Newborn

A
  • jaundice that arises because the newborn liver has transiently low UGT activity
  • the result is an increase in UCB within the blood
  • UCB is fat soluble so it can be deposited in the basal ganglia, a phenomenon known as kernicterus, which leads to neurologic deficits and death
  • treatment is phototherapy, which makes UCB water soluble and it is excreted in the urine
  • however, it usually resolves without treatment in 1-2 weeks
238
Q

What is kernicterus?

A

a complication sometimes seen in newborns because unconjugated bilirubin builds up in the blood and is fat soluble so it is deposited in the basal ganglia leading to neurologic deficits and death

239
Q

Gilbert Syndrome

A
  • an autosomal recessive condition characterized by mildly diminished UGT activity
  • results in a mild elevation of UCB during times of stress
  • not normally significant clinically
  • the mild version of Crigler-Najjar syndrome
240
Q

Crigler-Najjar Syndrome, Type I

A
  • the absence of UGT, which leads to extremely high levels of unconjugated bilirubin in the blood
  • often leads to Kernicterus in the early days of life
  • treatment involves plasmapheresis and phototherapy, but is usually fatal
241
Q

Dubin-Johnson syndrome

A
  • a deficiency of the bilirubin canalicular transport protein required for hepatocytes to move CB into the canaliculi
  • results in elevated conjugated bilirubin in the blood
  • the liver becomes pitch black but otherwise this is not clinically significant; it is often an incidental finding during surgery
  • Rotor syndrome is similar but lacks liver discoloration
242
Q

What would cause conjugated bilirubin levels in the blood to rise as well as an elevation of alkaline phosphatase?

A

biliary tract obstruction (aka obstructive jaundice), which will cause CB to leak into the blood rather than moving into the GI tract and which damages the wall and causes the release of alkaline phosphatase

243
Q

Obstructive Jaundice

A
  • biliary tract obstruction due to gallstones, carcinoma, parasites, or liver fluke leading to jaundice
  • the obstruction prevents conjugated bilirubin from entering the GI tract, so it leaks into the blood instead
  • urine will be dark with bilirubin rather than urobilinogen and urine urobilinogen will be low and stools pale
  • there is pruritus due to an increase in plasma bile acids, hypercholesterolemia with xanthomas, and steatorrhea with malabsorption of fat-soluble vitamins
  • labs show elevated direct (CB) bilirubin, reduced urine urobilinogen, and an increase in alkaline phosphatase
244
Q

Describe how the jaundice caused by viral hepatitis compares to other causes of jaundice.

A
  • arises because inflammation disrupts hepatocytes and small bile ductules
  • contributes to an increase in both conjugated bilirubin and unconjugated bilirubin because less bilirubin is conjugated and that which is doesn’t leave via the GI tract, instead it leaks into the blood
  • urine is dark due to an increase in urine bilirubin, but urine urobilinogen is normal or decreased
245
Q

Viral Hepatitis

A
  • an inflammation of liver parenchyma, most often due to hepatitis virus, but occasionally to EBV or CMV
  • the acute phase lasts less than six months and presents as jaundice (elevated UCB and CB) with dark urine, fever, malaise, nausea, and elevated liver enzymes (ALT > AST)
  • inflammation during the acute phase involves the lobules of the liver and portal tracts and triggers CD8 mediated apoptosis of hepatocytes
  • the chronic phase is that which lasts more than six months
  • during the chronic phase, inflammation predominantly involves the portal tract
  • chronic hepatitis increases the risk for cirrhosis
246
Q

How does the inflammation during acute hepatitis differ from that seen in chronic hepatitis?

A

in the acute phase, the inflammation involves lobules of the liver and portal tracts, but during the chronic phase, it predominantly involves the portal tracts

247
Q

Hepatitis A

A
  • an infection spread by fecal-oral transmission, most commonly acquired during travel outside the US
  • causes only acute hepatitis without a risk for chronic hepatitis
  • anti-virus IgM marks an active infection while anti-virus IgG is protective and indicates prior infection or immunization, which is available for HAV
248
Q

Hepatitis E

A
  • an infection spread by fecal-oral transmission and is commonly acquired from contaminated water or undercooked seafood
  • poses no risk for chronic hepatitis
  • anti-virus IgM marks an active infection while anti-virus IgG is protective and indicates prior infection
  • there is no vaccination available
  • importantly, in a pregnant woman, HEV is associated with fulminant hepatitis
249
Q

What is fulminant hepatitis?

A

a complication of HEV infection in a pregnant women characterized by liver failure with massive liver necrosis

250
Q

Hepatitis C

A
  • an infection spread via parenteral transmission

- results in an acute hepatitis that only occasionally progresses to chronic disease

251
Q

Hepatitis B

A
  • an infection spread via parenteral transmission
  • results in acute hepatitis and chronic hepatitis in most cases
  • HCV-RNA test confirms infection and decreased RNA levels indicate recovery
252
Q

What is unique about Hepatitis D?

A

infection with HDV is dependent on a simultaneous or pre-existing infection with HBV

253
Q

Which is worse, hepatitis B/D superinfection or co-infection?

A

superinfection (B and then D) is more severe

254
Q

Describe the antigen and antibody profile of someone with an acute HBV infection.

A
  • HBsAG is the first marker to rise
  • HBeAG and HBV DNA are also positive, and indicate infection
  • IgM to HBc is present
255
Q

Describe the antigen and antibody profile of someone with an chronic HBV infection.

A
  • HBsAG is present
  • HBeAG may or may not be present
  • IgG to HBc is present and antibody to HBs is absent
256
Q

What does the presence of HBsAg in an individual indicate?

A

it is the first serologic marker to rise in those with an HBV infection and it is indicative of present infection, either acute or chronic

257
Q

What does the presence of HBeAg or HBV DNA in an individual indicate?

A
  • it is a marker of infectiousness, so it is positive during the acute phase and can be positive or negative during the chronic phase
  • it is absent in all other phases
258
Q

What do IgM and IgG against HBc indicate in an individual being assessed for hepatitis?

A
  • IgM is seen only in the acute and window stages early in infection
  • IgG is seen in the later phases (chronic infection or resolution)
  • importantly no such antibodies are seen in individuals who have only been immunized and not exposed to HBV
259
Q

What does the presence of antibodies to HBs indicate in an individual being assessed for hepatitis?

A

it is protective and as such, is seen in those with resolved past infection and who have been immunized

260
Q

Those who have been immunized against HBV have what antibodies?

A

IgG against HBs

261
Q

Cirrhosis

A
  • end-stage liver damaged characterized by disruption of the normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes
  • mediated by TGF-B from stellate cells that line the sinusoids
  • presents with portal hypertension, which manifests as ascites, congestive splenomegaly, and portosystemic shunts
  • presents with decreased detoxification which manifests as mental status change, asterisks, and eventual coma due to elevated serum ammonia; gynecomastia, spider angiomata, and palmar erythema due to hyperestrinism; and jaundice
  • presence with decreased protein synthesis manifesting as hypoalbuminemia with edema and a coagulopathy
262
Q

Alcohol-Related Liver Disease

A
  • damage to the liver parenchyma due to alcohol consumption
  • can produce three patterns of injury: fatty liver, alcoholic hepatitis, or cirrhosis
  • fatty liver is the accumulation of fat in hepatocytes and grossly the liver becomes heavy and greasy; this resolves with abstinence
  • alcoholic hepatitis results from chemical injury to hepatocytes and is generally seen with binge drinking; the primary mediator of this is the ethanol metabolite acetaldehyde; hepatocytes swell and Mallory bodies (damaged cytokeratin filaments) form; notably AST > ALT
  • cirrhosis is a complication of long-term chronic alcohol-induced liver damage
263
Q

What does liver failure in the context of an AST more elevated than an ALT indicate?

A

it is indicative of alcoholic hepatitis because AST is found in the mitochondria and alcohol is a mitochondrial poison

264
Q

What are Mallory bodies?

A

aggregates of damaged cytokeratin filaments found in hepatocytes indicating alcoholic hepatitis

265
Q

Nonalcholic Fatty Liver Disease

A
  • fatty change, hepatitis, or cirrhosis that develop without exposure to alcohol or other known insult
  • associated with obesity
  • a diagnosis of exclusion
  • ALT more elevated than AST
266
Q

Hemochromatosis

A
  • organ damage due to excess iron in the body
  • usually due to an autosomal recessive C282Y mutation of the HFE gene on chromosome 6, which leads to abnormal iron sensing and increased intestinal absorption
  • secondary hemochromatosis may arise from chronic transfusion therapy
  • iron accumulates in the liver, pancreas, skin, heart, pituitary, and joints and can be identified on MRI or with a Prussian blue stain
  • presents after age 40 with a triad of cirrhosis, diabetes, and skin pigmentation (“bronze diabetes”) as well as restrictive cardiomyopathy, hypogonadism, arthropathy due to deposition of calcium pyrophosphate in the MCPs
  • HCC is a common cause of death
  • treat with phlebotomy and chelation
267
Q

What is the difference between hemosiderosis and hemochromatosis?

A
  • hemosiderosis is just the state of having elevated iron

- hemochromatosis is the organ damage that results

268
Q

What distinguishes iron deposits from lipofuscin?

A

iron deposits will stain using Prussian blue

269
Q

Wilson Disease

A
  • an autosomal recessive mutation in the hepatocyte copper-transporting ATPase gene ATP7B on chromosome 13
  • this defect prevents incorporation of copper into apoceruloplasmin for transport in the blood and into bile for excretion
  • instead, copper accumulates in the liver, brain, cornea, and kidneys
  • it presents before age 40 with cirrhosis, neurologic changes (including Parkinsonian symptoms from deposition in the basal ganglia), Kayser-Fleisher rings (deposits in the Descemet membrane of the cornea), hemolytic anemia, and Fanconi syndrome
  • labs show elevated urine copper and low serum ceruloplasmin
  • increases the risk for hepatocellulr carcinoma
  • treat with penicillamine or trientine and oral zinc
270
Q

Primary Biliary Cirrhosis

A
  • autoimmune granulomatous destruction of intrahepatic bile ducts
  • antimitochondrial antibodies are present but do not mediate the disease
  • presents with obstructive jaundice and cirrhosis later in the disease course
271
Q

Primary Sclerosing Cholangitis

A
  • inflammation and fibrosis of intrahepatic and extra hepatic bile ducts
  • histology reveals an onion-skin appearance of the periductal fibrosis and a beaded appearance on contrast imaging because uninvolved segments dilate
  • associated with ulcerative colitis and p-ANCA is often positive but the etiology is unknown
  • presents with obstructive jaundice and cirrhosis is a late complication
  • patients are at increased risk for cholangiocarcinoma
272
Q

Reye Syndrome

A
  • fulminant liver failure and encephalopathy in children with a viral illness who take aspirin
  • likely due to mitochondrial damage within hepatocytes; aspirin metabolites reduce beta-oxidation by reversible inhibition of mitochondrial enzymes
  • presents with hypoglycemia, fatty liver, n/v, hepatomegaly, and coma
  • Reye of sunSHINE: steatosis of liver, hypoglycemia/hepatomegaly, infection, not away (coma), encephalopathy
273
Q

Why are children with a viral illness never given aspirin? What disease complicates this general rule?

A
  • because it may induce Reye syndrome of fulminant liver failure and encephalopathy
  • this is complicated by Kawasaki disease with looks viral but is not and is treated with aspirin
274
Q

Hepatic Adenoma

A
  • a benign tumor of hepatocytes
  • associated with oral contraceptive use grows during pregnancy because it responds to estrogen
  • they are sub capsular but risk rupture and intraperitoneal bleeding during pregnancy for this reason
275
Q

Hepatocellular Carcinoma

A
  • a malignant tumor of hepatocytes
  • risk factors include chronic hepatitis, cirrhosis (secondary to alcohol, nonalcoholic fatty liver disease, hemochromatosis, Wilson disease, A1AT deficiency), and aflatoxins
  • tumors are often detected late because the symptoms are masked by cirrhosis
  • symptoms include jaundice, tender hepatomegaly, ascites, polycythemia, and anorexia
  • primarily complication is Budd-Chiari syndrome (liver infarction secondary to hepatic vein obstruction)
  • primary serum marker is alpha fetoprotein
276
Q

What are aflatoxins and why are they clinically important?

A

they are derived from Aspergillus which grows in stored grains and the toxin induces p53 mutations, increasing the risk for hepatocellulr carcinoma

277
Q

What serum marker is useful in diagnosing HCC?

A

alpha-fetoprotein

278
Q

What is Budd-Chiari syndrome?

A
  • liver infarction secondary to hepatic vein obstruction
  • presents with painful hepatomegaly and ascites
  • often complicates hepatocellulr carcinoma when the tumor invades the hepatic vein
279
Q

What are the most common sources of metastasis to the liver?

A

colon, pancreas, lung, and breast

280
Q

How do metastases to the liver often compare to primary cancers in gross appearance?

A

metastases result in multiple nodules in the liver whereas a primary tumor is more likely to arise as one lesion

281
Q

How can metastasis to the liver present on physical exam?

A

may be able to palpate the hepatomegaly as a nodular free edge of the liver (due to multiple nodules of tumor)

282
Q

Eosinophilic Esaphagitis

A
  • an infiltration of the esophagus by eosinophils, most often in patients with atopy
  • presents with dysphagia and food impaction for food allergens
  • can see esophageal rings and linear furrows on endoscopy
  • doesn’t respond to GERD therapy
283
Q

Esophagitis

A
  • an infection of the esophagus
  • commonly associated with reflux, immunocompromised hosts, caustic ingestion, or medications
  • Candida will presents as white pseudomembranes, HSV-1 as punched out ulcers, and CMV as linear ulcers
284
Q

Sclerodermal Esophageal Dysmotility

A
  • smooth muscle atrophy of the esophagus
  • results in reduced LES pressure and dysmotility, which contribute to acid reflux and dysphagia
  • complications include stricture, Barrett esophagus, and aspiration
  • a feature of CREST syndrome
285
Q

Menetrier Disease

A
  • hyperplasia of the foveolar cells of the gastric mucosa mediated by excess TGF-a
  • results in hypertrophied rugae, which take on the appearance of brain gyro on imaging, excess mucus production with resultant protein loss, and parietal cell atrophy with low acid production
  • considered precancerous
286
Q

What is a sister mary joseph nodule?

A

a subcutaneous periumbilical metastasis (often from diffuse or intestinal gastric carcinoma)

287
Q

How do we detect fecal fat in those with a malabsorption syndrome?

A

a Sudan stain

288
Q

Lactose Intolerance

A
  • a deficiency in lactase, which normally breaks lactose down into glucose and galactose
  • can be congenital via an AR mutation, acquired most often in late childhood, or transient following infection of the small bowel
  • villi appear normal unless it is secondary to injury to the tips of the villi as in viral enteritis
  • lactose remains in the lumen and causes an osmotic diarrhea with low stool pH since it is fermented by colonic bacteria
  • diagnosed via a lactose hydrogen breath test which is positive for malabsorption if post lactose breath hydrogen rises more than 20 ppm above base
289
Q

What is the lactose hydrogen breath test?

A
  • a test used to diagnose lactose intolerance
  • works on the basis that lactose that isn’t broken down and absorbed is formed in the colon by bacteria, increasing [H+]
  • positive if breath hydrogen rises more than 20 ppm after lactose is administered orally
290
Q

Pancreatic Insufficiency

A
  • a deficiency of pancreatic secretions
  • dueto chronic pancreatitis, CF, or obstructing cancer
  • results in a malabsorption of fat and fat-soluble vitamins as well as B12
  • low duodenal pH and fecal elastase are indicative signs
291
Q

The differential for appendicitis should include what else?

A
  • diverticulitis if elderly

- ectopic pregnancy if a young woman

292
Q

What is the most common congenital anomaly of the GI tract?

A

Meckle diverticulum

293
Q

What is an omphalomesenteric cyst?

A

a cystic dilation of the vitelline duct, related to Meckel diverticulum

294
Q

What is a pertechnetate study?

A

a diagnostic study for Meckel diverticulum that relies on uptake by ectopic gastric mucosa

295
Q

Zenker Diverticulum

A
  • a false pharyngoesophageal diverticulum
  • caused by dysmotility, which results in herniation of mucosal tissue at the Killian triangle between the tyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor
  • results in dysphagia, obstruction, gurgling, aspiration, foul breath, and a neck mass
  • most often seen in elderly males
296
Q

What are Ladd bands?

A

fibrous bands that form due to improper positioning of the bowel, which can lead to volvulus or duodenal obstruction

297
Q

What is the most common cause of small bowel obstruction?

A

adhesion

298
Q

Ileus

A
  • intestinal hypo motility in the absence of obstruction
  • presents with a distended/tympanic abdomen with diminished bowel sounds
  • often after abdominal surgeries, opiates, hypokalemia, or sepsis
  • treat with bowel rest, electrolyte correction, or a cholinergic drug
299
Q

Meconium Ileus

A

a feature of cystic fibrosis in which a meconium plug obstructs the small intestine, preventing stool passage at birth

300
Q

Necrotizing Enterocolitis

A
  • necrosis of the intestinal mucosa, most often the colon
  • seen in premature, formula-fed infants with immature immune systems
  • complicated by possible perforation, which can lead to pneumatosis intestinal, free air in abdomen, or portal venous gas
301
Q

What happens to albumin, prothrombin time, and platelets in those with liver disease?

A
  • albumin is decreased
  • there is a coagulopathy from reduced production of clotting factors, so prothrombin time increases
  • platelets are decreased in liver disease due to low thrombopoietin and liver sequestration and in portal hypertension due to splenic sequestration
302
Q

What causes platelets to decrease in those with liver disease?

A
  • liver disease results in low thrombopoietin production and liver sequestration of platelets
  • portal hypertension leads to splenomegaly and splenic sequestration
303
Q

Hepatic Encephalopathy

A
  • encephalopathy that results from cirrhosis, which diminishes ammonia metabolism
  • presentation can range from disorientation with asterisks to severe coma
  • may be triggered by increased ammonia production and absorption (dietary protein, GI bleed, constipation, or infection) or reduced ammonia removal (renal failure, diuretics, TIPS)
  • treat with lactulose which increases ammonium production or with rifaximin or neomycin which decrease ammonia-producing gut bacteria
304
Q

Cavernous Hemangioma

A
  • a common, benign tumor of the liver
  • typically occurring between the ages of 30-50
  • biopsy is contraindicated by the risk of hemorrhage
305
Q

How do Crigler-Najjar syndrome type I and II differ?

A
  • type II is less severe

- because of this it responds to phenobarbital, which increases liver enzyme synthesis

306
Q

Secondary Biliary Cirrhosis

A
  • extrahepatic biliary obstruction, which increases pressure in the intrahepatic ducts and leads to injury, fibrosis, and bile stasis
  • primarily arises in those with known obstructive lesions such as gallstones, biliary strictures, or pancreatic carcinoma
  • may be complicated by ascending cholangitis
307
Q

What are the risk factors for gallstones?

A

the 4 F’s

  • female
  • fat
  • fertile (pregnant)
  • forty
308
Q

What is the difference between a black and a brown gallstone?

A
  • black are radiolucent and formed from calcium, bilirubinate, and hemolysis
  • brown are radiopaque and indicative of infection
309
Q

What is the Charcot triad of cholangitis?

A

jaundice, fever, and RUQ pain

310
Q

What is a positive Murphy sign?

A

inspiratory arrest on RUQ palpating due to pain, indicating cholecystitis

311
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED
- Idiopathic

  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune disease
  • Scorpion sting
  • Hypercalcemia/Hypertriglyceridemia
  • ERCP
  • Drugs (sulfa, NRTIs, protease inhibitors)
312
Q

What is Trousseau syndrome?

A

a migratory thrombophlebitis presenting with redness and tenderness on palpitation of extremities, indicative of malignancy

313
Q

What are the mechanisms, uses, and adverse effects of aluminum hydroxide?

A
  • it is an antacid
  • used to treat gastric acid diseases
  • can cause hypokalemia, constipation, hypophosphatemia, proximal muscle weakness, osteodystrophy, and seizures
314
Q

What are the mechanisms, uses, and adverse effects of calcium carbonate?

A
  • it is an antacid
  • used to treat gastric acid diseases
  • can cause hypokalemia, hypercalcemia, and rebound acid secretion
315
Q

What are the mechanisms, uses, and adverse effects of magnesium hydroxide?

A
  • it is an antacid
  • used to treat gastric acid diseases
  • can cause hypokalemia, diarrhea, hyporeflexia, hypotension, and cardiac arrest
316
Q

What are the mechanisms and uses of bismuth and sucralfate?

A
  • they bind to the base of an ulcer and provide physical protection while bicarb secretion re-establishes the pH gradient in the mucous layer
  • used to treat ulcers and travelers’ diarrhea
317
Q

What are the mechanisms, uses, and adverse effects of misooprostol?

A
  • it is a PGE1 analog, which increase production and secretion of the gastric mucous barrier while limiting acid production
  • it is used to prevent NSAID-induced peptic ulcers, maintenance of a PDA, and induction of labor/as an abortifacient
  • may cause diarrhea or abortion
318
Q

What are the mechanisms, uses, and adverse effects of osmotic laxatives? List four examples.

A
  • magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose
  • provide an osmotic load to draw water into the GI lumen
  • used to treat constipation
  • may cause diarrhea or dehydration and may be abused by bulimics
319
Q

What are the mechanisms, uses, and adverse effects of sulfasalazine?

A
  • it is a combination of sulfapyridine and 5-aminosalicylic acid (anti-bacterial and anti-inflammatory), which is activated by colonic bacteria
  • used to treat UC and Crohn disease (if it affects the colon)
  • may cause malaise, nausea, sulfa toxicity, and a reversible oligospermia
320
Q

What are the mechanisms, uses, and adverse effects of Loperamide?

A
  • it is an agonist at mu receptors with very little CNS penetration
  • used to treat diarrhea
  • may cause constipation or nausea
321
Q

What are the mechanisms, uses, and adverse effects of orilstat?

A
  • a weight loss medication that functions by inhibiting gastric and pancreatic lipase, reducing the breakdown and absorption of dietary fats
  • may cause steatorrhea and a fat-soluble vitamin deficiency
322
Q

What are the mechanisms, uses, and adverse effects of ursodiol?

A
  • it is a nontoxic bile acid that improves bile secretion and reduces cholesterol secretion and reabsorption
  • used to treat primary biliary cirrhosis as well as to prevent or dissolve gallstones

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