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Gastrointestinal Flashcards

1
Q

Midgut development

A

The midgut is the lower duodenum to the 2/3 transverse colon

6th week- physiologic midgut herniates though umbilical ring

10th week-returns to abdominal cavity and rotates around superior mesenteric artery for total 270 counterclockwise

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2
Q

Where is the defect in gastroschisis and omphaloceles during development?

A

lateral fold closure

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3
Q

extrusion of abdominal contents through abdominal folds (R of umbilicus) NOT covered by peritoneum or amnion?

A

Gastroschisis

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4
Q

Failure of lateral walls to migrate at umbilical ring results in persistent midline herniation of abdominal contents into umbilical cord. Gut contents are surrounded by peritoneum

A

Omphaloceles

“O” surrounds the gut

related to congenital anomalies

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5
Q

What is the most common tracheoesophageal anomaly?

A

Esophageal atresia with distal tracheoesophageal fistulae

presents with polyhydramnios in utero because unable to swallow

vomit with first feeding

Air can enter the stomach compared to a pure EA where the stomach is gas less

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6
Q

Pt is a 1-2 day old baby with downs syndrome that presents with bilious vomiting and abdominal distention. What is this baby likely to have? what is the xray sign?

A

duodenal atresia due to failure to recanalze

double bouble on xray

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7
Q

Pt presents with bilious vomiting and abdominal distention within first 1-2 days of life and the apple peel sign on xray

A

jejunal and ileal atresia

disruption of mesenteric vessels leading to ischemic necrosis and segmental resorption (bowel discontinuity)

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8
Q

What is the most common cause of gastric outlet obstruction in infants?

A

hypertrophic pyloric stenosis

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9
Q

Infant presents with a palpable olive shaped mass in the epigastric region and nonbillious projectile vomiting with visible peristaltic waves at 2-6 wks old

A

Hypertrophic pyloric stenosis

more in firstborn males
associated withe exposure to macrolides

vomiting empties gastric acid and results in hypokalemic and hypochloremic metabolic alkalosis

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10
Q

What becomes the body, tail, isthmus and accessory pancreatic duct?

A

dorsal pancreatic bud

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11
Q

What becomes the pancreatic head?

A

Both dorsal and ventral pancreatic bud

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12
Q

What becomes the uncinate process and the main pancreatic duct?

A

ventral pancreatic bud

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13
Q

Annular pancreas

A

abnormal rotation of ventral pancreatic bud results in a ring formation that encircles the second part of the duodenum causing duodenal narrowing and vomiting

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14
Q

When the ventral and dorsal buds fail to fuse at 8 weels

A

pancreas divisum

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15
Q

What is the spleen derived from?

A

mesoderm but has foregut supply from celiac trunks splenic artery

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16
Q

retroperitoneal organs

A 
suprarenal/adrenal glands
Aorta/IVC
Duodenum (2nd through 4th part)
Pancreas (except tail)
Ureters
Colon (descending and ascending)
Kidneys
Esophagus (thoracic portion)
Rectum (partially)

“SAD PUCKER”

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17
Q

Falciform ligament

A

liver to anterior abdominal wall

contains the ligmentum teres hepatis and patent paraumbilical veins

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18
Q

Hepatoduodenal ligament

A

Liver to duodenum

contains the portal triad: proper hepatic artery, portal vein, common bile duct

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19
Q

Pringle manuver

A

Hepatoduodenal ligament may be compressed between thumb and index finger placed in omental foramen to control bleeding

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20
Q

Gatrohepatic ligament

A

liver to less curvature of stomach

contains the gastric vessels

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21
Q

Gatrocolic ligament

A

connects greater curvature and transverse colon

contains the gastroepiploic arteries

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22
Q

Gastrosplenic ligament

A

connects the greater curvature and spleen

contains teh short gastrics, left gastroepiploic vessels

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23
Q

Splenorenal ligament

A

connects the spleen to posterior abdominal wall

contains the splenic artery and vein, tail of pancreas

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24
Q

Layers of gut wall

A

Mucosa- epithelium –> lamina propria–> muscularis mucosa

submucosa- submucosal nerve plexus (meissner)

Muscularis externa - inner circular mm, myenteric nerve plexus (auerbach), outer longitudinal mm

Serosa if intraperitoneal/adventitia if retroperitoneal

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25
Q

Cell type in the esophagus?

A

nonkeratinized stratified squamous epithelium

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26
Q

Brunners glands

A

In duodenum

HCO3 secreting cells of submucosa

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27
Q

Crypts of lieberkuhn

A

In duodenum, jejunum, ileum, colon

contains stem cells ( in duodenum they can replace enterocytes/goblet cells and paneth cells tat secrete defensins, lysozyme, and TNF)

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28
Q

Plicae circulares

A

In distal duodenum, jejunum, proximal ileum

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29
Q

Peyers patches

A

in ileum

lymphoid aggregates in lamina propria and submucosa

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30
Q

Largets number of goblet cells in the small intestine is in the?

A

ileum

Colon also has abundant goblet cells

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31
Q

Vertebral levels of major abdominal arteries - celiac trunk, SMA, IMA? Bifurcation of aorta?

A

celiac- T12
SMA-L1
IMA-L3

Bifurcation of aorta at L4 “biFOURcation”

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32
Q

In low body weight patients, we worry about superior mesenteric artery syndrome…which is?

A

characterized by intermittent intestinal obstruction symptoms primarily post prandial pain

when SMA and aorta compress transverse (3rd) part of duodenum

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33
Q

Where is the colon prone to ischemia?

A

at watershed areas where you get distal arterial branches

1) splenic flexure -SMA and IMA
2) rectosigmoid junction - the last sigmoid arterial branch from the IMA and superior rectal artery

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34
Q

blood supply and innervation of foregut? midgut? hindgut?

A

foregut is celiac artery with parasymp innervation from vagus

Midgut is SMA with parasympathetic innervation from vagus

Hindgut is IMA with pelvic parasympathetics

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35
Q

Branches of celiac trunk?

A

hepatic, splenic, left gastric

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36
Q

Posterior duodenal ulcers run the risk of penetrating what artery and causing hemorrhage?

A

gastroduodenal artery

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37
Q

What is the risk with anterior duodenal ulcers?

A

perforate into the anterior abdominal cavity and potentiall lead to pneumoperitoneum

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38
Q

portal systemic anastomoses: esophagus

A

left gastric with azygos

clinical sign is esophageal varices

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39
Q

portal systemic anastomoses: umbilicus

A

paraumbilical with small epigastric veins of ant ab wall

clinical sign is caput medisae

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40
Q

portal systemic anastomoses: rectum

A

superior rectal with middle and inferior rectal

clinical sign is anorectal varices

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41
Q

Anorectal varices, caput medusae, esophageal varices are commonly seen with

A

portal HTN

TX then with transjugular intrahepatic portosystemic shunt (TIPS) between portal and hepatic vein that shunts blood to the systemic circulation, bypassing liver and reducing portal HTN

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42
Q

What is the pectinate/dentate line? why is it important?

A

where the endoderm (hindgut) meets ectoderm

above line: internal hemorrhoids (not painful because visceral innervation), adenocarcinoma

below line: external hemorrhoids (painful because somatic innervation from inferior rectal branch of pudendal nerve), anal fissures, squamous cell carcinoma

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43
Q

Anal fissures are most commonly located?

A

below pectinate line

posteriorly because poorly perfused

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44
Q

Liver tissue function unit and struture

A

the functional unit of the liver is made up of hexagonally arranged lobules surrounding the central vein with portal triads on the edges (consisting of portal vein, hepatic artery, bile ducts, lymphatics)

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45
Q

Kupffer cells

A

specialized macrophages in liver

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46
Q

Hepatic stellate (Ito) cells

A

in space of Disse store vitamin A and produce extracellular matrix when activated –> hepatic fibrosis

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47
Q

Liver zones

A

Zone I: perioportal zone - affected first by viral hepatitis and ingested toxins

Zone II: intermediate zone - related to yellow fever

Zone III: pericentral vein (Centrilobular)zone - affected first by ischemia, high cytochrome P450, most sensitive to metabolic toxins, site of alcoholic hepatitis

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48
Q

Tumors of the head of the pancrease commonly cause?

A

obstruction of the common bile duct that results in enlarged gallbladder with painless jaundice (courvoisier sign)

commonly andenocarcinoma

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49
Q

Femoral structures from lateral to medial? Whats in the femoral triangle? Femoral sheath?

A
  • Nerve-Artery-Vein-Lymphatics - “NAVeL”
  • NAV is in the femoral triangle - “Venous near the penis”
  • sheath that is below the inguinal ligament that contains femoral vein, artery, and canal (deep inguinal lymph nodes) but not femoral nerve
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50
Q

Muscles of the inguinal canal

A

Transversus abdominis mm
Internal oblique mm

which fuse into a conjoined tenden

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51
Q

Spermatic cord structure

A

ICE tie

Internal spermatic fascia (transversalis fascia)
Cremasteric muscle and fascia (internal oblique)
External Spermatic fascia (external oblique)

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52
Q

Hesselbach triangle

A

Inguinal triangle

  • inferior epigastric
  • lateral border of ther ectus abdominis
  • inguinal ligament
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53
Q

Diaphragmatic hernia? where is it more common?

A

abd structures enter the thorax. mostly on the left side because the liver protects the right side

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54
Q

Most common diaphragmatic hernia? What is the other type?

A
  • sliding hiatal hernia is most common. The GE junction is displaced upward as gastric cardia slides into the esophageal hiatus . “hourglass stomach”
  • paraesophageal hiatal hernia is when the gastric fundus herniates
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55
Q

This type of hernia follows the path of descent of the testes and is covered by all 3 layers of spermatic fascia

A

Indirect inguinal hernia - Lateral to inferior epigastrics (MDs dont LIe - medial is direct hernia, Lateral is indirect)

goes through the internal (deep) inguinal ring, external (superficial) inguinal ring, and into the scrotum

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56
Q

What causes an indirect inguinal hernia?

A

caused by failure of processus vaginalis to close and can form a hydrocele

more common in males

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57
Q

This type of hernia protrudes through the inguinal triangle

A

Direct inguinal hernia bulges directly though parietal peritoneum medial to the inferior epigastric vessels but lateral to rectus abdominis

ONLY goes through external (superficial) inguinal ring

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58
Q

This hernia protrudes below the inguinal ligament through the femoral canal below and lateral to pubic tubercles

A

Femoral hernia

mostly females

more likely to present with incarceration or strangulation than inguinal hernias

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59
Q

Gastrin

A
  • From G cells of the antrum of stomach and duodenum
  • increases H+ gastric secretion
  • Increases gastric mucosa growth and motility

effect is due to enterochromaffin-like cells (ECL) that leads to histamine release rather than through its direct effect on parietal cells

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60
Q

Somatostatin

A
  • From D cells in pancreatic islets and GI mucosa
  • Decrease gastric acid and pepsinogen secretion
  • Decrease pancreatic and small intestine fluid secretion
  • Decrease gallbladder contraction
  • Decrease insulin and glucagon release

high acidity induces release

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61
Q

Cholecystokinin

A
  • From I cells in duodenum and jejunum
  • Increase pancreatic secretion
  • Increase gallbladder contraction
  • Decrease gastric emptying
  • Increase sphincter of Oddi relaxation
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62
Q

Secretin

A
  • From S cells in the duodenum
  • Increase pancreatic HCO3 secretion
  • decrease gastric acid secretion
  • increase bile secretion
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63
Q

Glucose-dependent insulinotropic peptide/gastric inhibitory peptide (GIP)

A
  • From K cells (duodenum, jejunum)
  • exocrine: decrease gastric H+ secretion
  • endocrine: increase insulin release
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64
Q

Motilin

A
  • From small intestine

- Produces migrating mtoor xomplexes (MMCs)

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65
Q

Vasoactive Intestinal Polypeptide

A
  • From parasympathetic ganglia in sphincters, gallbladder, small intestine
  • Increase intestinal water and electrolyte secretion
  • Increase relaxation of intestinal smooth mm and sphincters
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66
Q

Nitric Oxide

A
  • increase smooth muscle relaxation, including lower esophageal sphincter
  • Loss of NO related to achalasia’s increase lower esophageal sphincter tone
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67
Q

Ghrelin

A
  • From stomach

- Increases appetite

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68
Q

Intrinsic factor

A
  • From parietal cells of stomach

- Vitamin B12 binding protein (required for B12 uptake in terminal ileum)

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69
Q

Gastric acid

A
  • From parietal cells of stomach
  • Decreases stomach pH
  • Regulation: increases with histamine, vagal stimulation (ACh), gastrin. Decreases with somatostatin, GIP, secretin
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70
Q

Pepsin

A

-From chief cells (Stomach)
-Protein digestion
REgulation: increase by vagal stimulation (ACh)

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71
Q

Bicarbonate

A
  • From mucosal cells in stomach, duodenum, salivary glands, pancreas and brunners glands in duodenum
  • Neutralizes acid
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72
Q

Pancreatic alpha amylase

A

starch digestion

released in active form

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73
Q

Pancreatic lipases

A

fat digestion

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74
Q

Panctreatic proteases

A

protein digestion

trypsin, chymotrypsin, elastase, carboxypeptidases which are secreted as proenzymes

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75
Q

Pancreatic trypsinogen

A

converted to active trypsin (by enterokinase/enteropeptidase on brush border)

which then goes on to activate other proenzymes and cleaving of additional trypsinogen molecules into active trypsin

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76
Q

Where is Fe absorbed? Folate (B9)? B12?

A
  • duodenum for Fe
  • small bowel for folate
  • terminal ileum for B12
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77
Q

Peyers patches

A
  • unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum
  • specialized M cells sample and present antigens to immune cells
  • B cells in germinal centers differentiate into IgA secreting plasma cells which will reside in lamina propria
  • IgA receives protective secretory component and is then transported across epithelium to deal with intraluminal antigens
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78
Q

What are bile acids conjugates to

A

glycine

taurine

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79
Q

What is teh rate limiting step of bile acid synthesis

A

cholesterol 7alpha hydroxylase

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80
Q

Low bile salt absorption can result in what kind of stones and why

A

calcium oxalate kidney stones

Ca which normally binds oxalate, binds fat instead and so free oxalate is absorbed by gut and causes stones

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81
Q

Bilirubin pathway

A

1) macrophages break down RBCs and release heme which is metabolized by heme oxygenase to biliverdin which is reduced to bilirubin
2) unconjugated bilirubin/indirect is water insoluble and is in macrophages
3) enters bloodstream and joins albumin to form unconjugated bilirubin albumin complex
4) enters liver and via UDP-glucuronosyl-transferase –> conjugated bilirubin/direct bilirubin/water soluble
5) gut bacteria turns this into urobilinogen which 80% excreted by feces as stercobilin (brown color) and rest either excreted in urine as urobilin (yellow color) or go to liver via enterohepatic circulation

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82
Q

Sialolithiasis

A

Stones in salivary gland

single stone more common in submandibular gland (wharton duct)

caused by dehydration or trauma

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83
Q

Sialadenitis

A

inflammation of salivary gland

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84
Q

Salivary gland tumors

A

most commonly benign and in parotid gland

presents as painless mass/swelling

Facial pain or paralysis suggests malignant involvement of CN VII

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85
Q

The most common salivary gland tumor

A

pleomorphic adenoma- benign mixed tumor of chondromyxoid stroma and epithelium

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86
Q

The most common malignant tumor of salivary gland

A

Mucoepidermoid carcinoma

has mucinous and squamous components

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87
Q

A benign cystic tumor of salivary gland with germinal centers

A

warthin tumor (papillary cystadenoma lymphomatosum)

seen in smokers
Bilateral in 10%
Multifocal in 10%

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88
Q

Barium swallow shows dilated esophagus with an area of distal stenosis “birds beak sign”

A

Achalasia-Failure of LES to relax due to loss of myenteric (auerbach) plexus due to loss of postganglionic inhibitory neurons (which contain NO and VIP)

Increased risk of esophageal cancer

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89
Q

Pt presents with crepitus felt in neck region and chest wall

A

Boerhaave syndrome

Transmural (compared with mallory weiss which is non transmural)

Distal esophageal rupture with pneumomediastinum due to violent retching

subq emphysema may be due to dissecting air

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90
Q

Infiltration of eosinophils in the esophagus

A

Eosinophilic esophagitis

esophageal rings and linear furrows often seen on endoscopy

unresponsive to GERD therapy

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91
Q

Esophageal strictures

A

Associated with caustic ingestion (Strong acid/base) and acid reflux

92
Q

Esophagitis

A

reflux, infection in immunocompromised (candida causes pseudomembrane, HSV-1 causes punched out lesion, CMV causes linear ulcers), caustic ingestion, or pill esophagitis

93
Q

Mallory Weiss syndrome

A

partial thickness mucosal lacerations at gastroesophageal junction due to severe vomiting

alcoholics and bulimics

94
Q

pt presents with triad of dysphagia, iron deficiency anemia, and esophageal webs

A

Plummer vinson syndrome

increased risk of esophageal squamous cell carcinoma

“Plumbers DIE”

95
Q

Pt presents with esophageal smooth muscle atrophy as part of CREST syndrome

A

Sclerodermal esophageal dysmotility

decreased LES pressure and dysmotility –> acid reflux and dysphagia –> stricture, barrett esophagus, and aspiration

96
Q

The replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (nonciliated columnar with goblet cells in distal esophagus)

A

Barrett esophagus

can cause esophageal adenocarcinoma

97
Q

Esophageal cancer that affects the upper 2/3rd of the esophagus and is most common worldwide

A

squamous cell carcinoma due to alcohol, hot liquids, caustic strictures, smoking, achalasia

98
Q

Esophageal cancer that affects the lower 1/3 of the esophagus and is most common in america

A

Adenocarcinoma due to chronic GERD, Barrett esophagus, obesity, smoking, achalasia

99
Q

Why do NSAIDs cause erosions in acute gastritis?

A

they decrease PGE2 which decreases gastric mucosa protection

100
Q

Curling ulcer in acute gastritis

A

Burns cause curling ulcer which has hypovolemia –> mucosal ischemia

“burned by the curling iron”

101
Q

Cushings ulcer in acute gastritis

A

Brain injury causes increase in vagal stimulation causes increase in ACh and thus H+ production

“always cushion the brain”

102
Q

hypochlorhydria

A

refers to states where the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low,

103
Q

H pylori in chronic gastritis

A

affects antrum first and spreads to body of stomach

worry about MALT lymphoma

104
Q

Menetrier disease

A

Hyperplasia of gastric mucosa causes hypertrophied rugae and causes excess mucus production with resultant protein loss and parietal cell atrophy with decrease acid production

precancerous

pt presents with epigastric pain, anorexia, weight loss, vomiting, edema (due to protein loss)

105
Q

Gastric cancers are commonly _____

A

adenocarcinoma

can present with acanthosis nigricans and leser trelat sign

Associated with blood type A

106
Q

Diffuse gastric cancer

A

signet ring cells (mucin filled cells with peripheral nuclei)

stomach wall grossly thickened and leathery (linitis plastica)

107
Q

Intestinal gastric cancer

A

commonly on lesser curvature and looks like ulcer with raised margins

108
Q

Virchow node

A

involvement of left supraclavicular node by metastasis from stomach

109
Q

Krukenberg tumor

A

bilateral metastases to ovaries. abundant mucin secreting signet ring cells

110
Q

Sister Mary joseph nodule

A

subq periumbilical metastasis

111
Q

affect of meals on gastric ulcer? duodenal ulcer?

A

Gastric ulcer - greater pain with meals + weight loss

duodenal ulcer-paind ecreases with meals + weight gain

112
Q

Ruptured gastric ulcer on the lesser curvature of stomach

A

bleeding from left gastric artery

113
Q

Ruptured ulcer on the posterior wall of duodenum

A

bleeding from gastroduodenal artery

114
Q

Duodenal hemorrhhaging is more common in post or ant?

A

post>ant

115
Q

Duodenal perforation is more common in aant or post?

A

ant>post

116
Q

Celiac disease/gluten sensitive enteropathy/celiac sprue

A

autoimmune mediated intolerance of gliadin protein in gluten –> malabsorption and steatorrhea. Can get dermatitis herpetiformis

117
Q

Celiac dz is associated with what HLA?

A

HLA-DQ2
HLA-DQ8

couldnt eat her 28 DQ icecreams

118
Q

pt presents with IgA anti tissue transglutaminase (IgA tTG), anti-endomysial, anti deamidated gliadin peptide antibodies

A

Celiac dz

  • villous atrophy
  • crypt hyperplasia
  • intrapeithelial lymphocytosis

primarly affects distal duodenum and or proximal jejunum

119
Q

Dxylose test

A

passive absorbed in proximal small intestine; blood and urine levels decrease with mucosa defects or bacterial overgrowth

120
Q

Lactose hydrogen breath test

A

positive for lactose malabsorption if post lactose breath hydrogen value rises>20 ppm compared with baseline

121
Q

Tropical sprue

A

similar to celiac sprue except responds to antibiotics

associated with megaloblastic anemia due to folate deficiency and later B12 deficiency

122
Q

Disease caused by Tropheryma Whipplei, an intracellular gram +

A

PAS + foamy macrophages in intestinal lamina propria

Whipple disease causes mostly in older men

cardiac symptoms
Arthralgias
Neurologic symptoms

“foamy whipped cream in a CAN”

123
Q

Crohns disease

A
  • Any portion of GI tract can be affected but mostly ileum and colon
  • Skip lesions with rectal sparring
  • transmural inflammation causing fistulas
  • Cobblestone mucosa, creeping fat, bowel wall thickening causes string sign on barium swallow xray
  • non caseating granulomas and lymphoid aggregates
  • Th1 mediated
  • kidney stones due to calcium oxalate and gallstones
    • anti-saccharomyces cerevisiae antibodies (ASCA)
124
Q

Ulcerative colotis

A
  • Continuous colonic lesions that extend proximally
  • Rectal involvement
  • mucosal and submucosal only
  • superficial and deep ulcerations
  • loss of haustra causes lead pipe appearance on imaging
  • bloody diarrhea
  • no granulomas
  • Th2 mediated
  • toxic megacolon
  • associated with primary sclerosing cholangitis (p-ANCA)
125
Q

Cause of appendicitis in adults? in children?

A

in adults its fecalith

In children its lymphoid hyperplasia

126
Q

Diverticulum

A

blind pouch protruding from the alimentary tract that communicates with the lumen of the gut

127
Q

Only mucosa and submucosa outpuch. Especially where the vasa recta perforate muscularis externa

A

if acquired then its a “false diverticula” or pseudodiverticulum

128
Q

All gut layers outpouch

A

True diverticulum (i.e. Meckels)

129
Q

Diverticulosis is common in the

A

sigmoid colon and caused by increase intraluminal pressure and focal weakness in colonic wall

can get painless hematochezia or diverticulitis –> LLQ, fever, leukocytosis

130
Q

Patient is an elder male with dysphagia, obstruction, gurgling, aspiration, foul breath, and a neck mass

A

Zenker diverticulum - pharyngoesophageal false diverticulum

esophageal dysmotility causes hernaition of mucosal tissue at killian triangle between the thyropharyngeal and cricopharyngeal parts of the inferior pharygneal constrictor

131
Q

Meckels diverticulum

A

true diverticulum

due to the persistence of the vitelline (omphalomesenteric) duct

findings: hematochezia, melena, RLQ pain, intussusception, volvulus, or obstruction near terminal ileum

132
Q

Rules of 2 for Meckels diverticulum

A 
2x more in males
2 inches long
2 feet from ileocecal valve
2% of population
first 2 years of life
2 types of epithelia (gastric and pancreatic)
133
Q

Patient presents with bilious emesis, abdominal distention, and failure to pass meconium within 48 hours (chronic constipation). A portion of the colon is dialated. Patient mentions having explosive expulsion of feces (squirt sign) and now has an empty rectum on digital exam

A

Hirschsprung disease

Congential megacolon that lacks gangion cells/enteric nervous plexus (auerbach and meissner plexuses) in distal segment of colon.

dilated portion is near the aganglionic segment and results in transition zone

risk increases with down syndrome

RET mutation int he RecTum

134
Q

Treatment for hirschsprung disease

A

is resection

135
Q

What is seen in the anomaly of improper midgut rotation

A

malrotation will show small bowel clumped on right side and colon on left

there is also formation of fibrous bands called ladd bands

can lead to volvulus and duodenal obstruction

136
Q

What causes the coffee bean sign on xray

A

sigmoid volvulus

twisting of portion of bowel around its mesentery which can lead to obstruction and infarction

137
Q

Type of volvulus seen in children? in elderly?

A

children see midgut volvulus

elderly see sigmoid volvulus which causes the coffee bean sign

138
Q

What is intussusception and where is it commonly seen?

A

telescoping of proximal bowel segment into the distal segment, commonly at ileocecal junction

139
Q

Patient presents with intermittent abdominal pain with currant jelly stools. Exam found a sausage shaped mass and the ultrasound showed the “target sign”

A

Intussusception

commonly due to Meckels diverticulum (children) or intraluminal mass (adults). Mostly children

can be related to Henoch Schonlein purpura, rotavirus, and recent viral infection where peyer patch hypertrophy creates lead point

140
Q

Patient presents with abdominal pain thats out of proportion to physical findings, also you note red currant jelly stools

A

Acute mesenteric ischemia - critical blockage of intestinal blood flow often due to embolic occlusion of SMA –> causing small bowel necrosis

141
Q

Patient has postprandial epigastric pain. She now has food aversion and weight loss

A

Chronic mesenteric ischemia - intestinal angina

atheroslerosis of celiac artery, SMA, or IMA causes intestinal hypoperfusion

142
Q

Pt has crampy abdominal pain followed by hematochezia. On imaging you notice a thumbprint sign due to mucosal edema/hemorrhage

A

colonic ischemia - reduction of intestinal blood flow causes ischemia. commonly at watershed areas (splenic flexure and distal colon)

elderly

143
Q

Angiodysplasia

A
  • tortuous dilation of vessels –> hematochezia
  • mostly found in R. sided colon
  • older patients
  • associated with aortic stenosis and von willebrand disease
  • confirmed with angiography
144
Q

What is the most common cause of small bowel obstruction?

A

adhesions

145
Q

Ileus

A

intestinal hypomotility without obstruction

146
Q

Meconium ileus is commonly seen in _____

A

in CF, meconium plug obstructs intestine, preventing stool passage at birth

147
Q

Necrotizing enterocolitis

A

Seen in premature formula fed infants with immature immune system

primarily colonic necrosis with possible perforation

can lead to pneumatosis intestinalis, free air in abdomen, portal venous gas

148
Q

Hamartomatous polyps

A

solitary lesions
no significant risk
normal colonic tissue with distorted architecture

associated with peutz-jeghers syndome and juvenile polyposis

149
Q

Inflammatory pseudopolyps are seen in ___

A

inflammatory bowel disease - mucosal erosions

150
Q

submucosal polyp examples

A

lipoma
leiomyomas
fibroma

151
Q

What polyp type is most common

A

hyperplastic polyps that can evolve into serratted polyps and more advanced lesions

mostly in rectosigmoid region

152
Q

adenomatous polyps

A

malignant potential (villous on histo > maligant potential than tubular)

mutations in APC and KRAS cause chromosomal instability

153
Q

Serrated polyps

A

Premalignant –> 20% colorectal cancer

“sawtooth pattern” of crypts on biopsy

CpG island methylator phenotype (CIMP; cytosine base followed by guanine)

Defect may silence the MMR gene. Mutations lead to microsatellite instability and mutations in BRAF

154
Q

thousands of polyps arise starting after puberty in a pancolonic fashion and always involves the rectum

A

Familial adenomatous polyposis –> 100% CRC

Autosomal dominant mutation of APC tumor suppressor gene on chromosome 5q21

give prophylactic colectomy

155
Q

Gardner syndrome (familial colorectal polyposis)

A

1) FAP + osseous and soft tissue tumors
2) congential hypertorphy of retinal pigment epithelium
3) impacted/supernumerary teeth

156
Q

Turcot syndrome

A

FAP/Lynch syndrome +malignant CNS tumor

157
Q

Autosomal dominant syndrome featuring numerous hamartomas throughout GI tract. Pt also has hyperpigmented mouth, lips, hands, genitalia

A

Peutz-Jeghers syndrome

associated with increased risk of breast and GI cancers

158
Q

Autosomal dominant syndrome in children <5 yo featuring numerous hamartomatous polyps in the colon, stomach, small bowel

A

Juvenile polyposis syndrome

associated with increased risk of CRC

159
Q

Lynch syndrome

A

Hereditary nonpolyposis colorectal cancer (HNPCC)

autosomal dominant mutation of DNA mismatch repair genes with subsequent microsatellite instability

80% progress to CRC and proximal colon is always involved

160
Q

Lynch syndrome is commonly associated with what cancers

A
  • endometrial
  • ovarian
  • skin cancers
161
Q

Colorectal cancer is most common in

A

Rectosigmoid>ascending>descending

if on the right side we see bleeding
If on the left side we see obstruction

see “apple core” on barium enema xray

162
Q

ascending colorectal cancer

A

exophytic mass
Iron deficieny anemia
weight loss

if man >50 yo or postmenopausal woman has iron deficiency anemia, you have high suspicion

163
Q

Descending colorectal cancer

A

infiltrating mass
partial obstruction
colicky pain
hematochezia

164
Q

Screening for colorectal cancer

A

at 40 yo if family history or 10 years before the family members presentation

normally starts at 50 yo

use CEA marker for monitoring recurrence

165
Q

Molecular pathogenesis of colorectal cancer

A

chromosomal instability pathway: mutations in APC cause normal colon to be at risk. Then a KRAS mutation will result in adenoma. Loss of tumor suppressor genes like p53 will result in carcinoma

APC loss causes decrease intercellular adhesion and increase proliferation

KRAS mutation causes unregulated intracellular signaling

Loss of tumor suppressor causes increase in tumorigenesis

166
Q

Mutations in FAP? mutations in lynch?

A

FAP is related to APC mutation (chromosomal instability pathway)

Lynch syndrome is mutation or methylation of mismatch repair genes like MLH1 (microsatellite instability pathway)

167
Q

This is a common and potentially fatal bacterial infection in patients with cirrhosis and ascites

A

spontaneous bacterial peritonitis also known as primary bacterial peritonitis

mostly aerobic gram negative orgnaisms

paracentesis of ascitic fluid absolute neutrophil count (ANC) >250

first line treatment is 3rd generation cephalosporin

168
Q

aspartate aminotransferase (AST)

A

AST>ALT in alcoholic liver disease

if AST>ALT in non alcoholic liver disease then worry it has progressed to advanced fibrosis or cirrhosis

169
Q

alanine aminotransferase (ALT)

A

ALT>AST in liver disease

170
Q

alkaline phosphatase

A

increases in cholestasis,infiltrative disorders, bone disease

171
Q

gamma glutamyl transpeptidase

A

increases in various liver and biliary diseases

but not in bone disease

associated with alcohol use

172
Q

Bilirubin

A

increases in liver dz

173
Q

Albumin

A

decreases in advanced liver dz

174
Q

Prothrombin time

A

increases in advanced liver disease because decrease in production of clotting factors

175
Q

Platelets

A

decrease in advanced liver disease (drop in thrombopoietin)

portal hypertension (splenomegaly/splenic sequestration)

176
Q

Rare often fatal childhood hepatic encephalopathy

A

reye syndrome

“reye of sunSHINE”

S-steatosis of liver/hepatocytes
H-hypoglycemia/hepatomegaly
I-Infection (VZV, influenza that has been treated with aspirin)
N-not awake (coma)
E (encephalopathy)

mitochondrial abnormalities
fatty liver due to microvesicular fatty change

177
Q

Why does aspirin increase the risk of reyes syndrome

A

aspirin decreases beta oxidation by reversible inhibition of mitochondrial enzymes

avoid in children unless have kawasaki disease

178
Q

Alcoholic hepatitis histo findings

A

swollen and necrotic hepatocytes with neutrophilic infiltration

mallory bodies- intracytoplasmic eosinophilic inclusions of damaged keratin filaments

179
Q

alcoholic liver disease progression

A

hepatic steatosis –> alcoholic hepatitis –> alcoholic cirrhosis

180
Q

Non alcoholic fatty liver disease

A

ALT>AST

metabolic syndrome (insulin resistance)

obesity –> fatty infiltration of hepatocytes –> cellular ballooning and eventual necrosis

may cause cirrhosis and HCC independent of alcohol use

181
Q

hepatic encephalopathy

A

cirrhosis causes a portosystemic shunt which decreases NH3 metabolism –> neuropsychiatric dysfunction

due to increased production and absorption OR decreased NH3 removal

treatment: lactulose if theres increased generation
and rifaximin or neomycin to decrease NH3 producing gut bacteria

182
Q

Findings seen in hepatocellular carcinoma/hepatoma and how to dx

A 
jaundice
tender hepatomegaly
ascites
polycythemia
anorexia
spreads hematogenously

dx due to increase alpha feto protein, ultrasound, contrast CT/MRI, biopsy

183
Q

The most common benign liver tumor that occurs at 30-50 yo. Do not biopsy because of risk of _____

A

cavernous hemangioma

do not because of hemorrhage risk

184
Q

What benign liver tumor is often related to oral contraceptibe or anabolic steroid use

A

hepatic adenoma

may regress or rupture (abd pain and shock)

185
Q

Liver tumor that malignant and related to arsenic and vinyl chloride exposure. Endothelial origin

A

Angiosarcoma

186
Q

Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis resulting in congestive liver disease. Risk in hepatocellular carcinoma/hepatoma, hypercoagulable states etc.

A

Budd chiari syndrome

hepatomegaly
ascites
varices
abd pain
liver failure
absence of JVD
may cause a nutmeg liver
187
Q

alpha1-antitrypsin deficiency

A

results in misfolded gene product protein aggregates in hepatocellular ER –> cirrhosis with PAS + globules in liver

young pt, liver damage, dyspnea, no history of smoking

188
Q

how does alpha1-antitrypsin deficiency affect the lings?

A

decrease in alpha1-antitrypsin causes uninhibited elastaste in alveoli and this decrease in elastic tissue and panacinar emphysema

189
Q

Jaundice is due to an increase in ______ and is caused by _______, ______, ______, ________

A

high bilirubin

think HOT liver

H-hemolysis
O-obstruction
T-Tumor
Liver disease

190
Q

Unconjugated (indirect) hyperbilirubinemia

A

hemolytic
physiologic (newborns)

crigler-najjar
Gilbert syndrome

191
Q

conjugated (direct) hyperbilirubinemia

A 
biliary tract obstruction
biliary disease (primary sclerosing cholangitis and primary biliary cholangitis)
excretion defects (dubin johnson syndrome or rotor syndrome)
192
Q

Mixed (direct and indirect) hyperbilirubinemia

A

hepatitis

cirrhosis

193
Q

Physiologic neonatal jaundice is due to immature _____

A

immature UDP-glucuronosyltransferase –> unconjugated hyperbilirubinemia –> jaundice/kernicterus (deposition of unconjugated lipid soluble bilirubin in the brain, particularly basal ganglia)

194
Q

Treatment for physiologic neonatal jaundice

A

phototherapy (non-UV) isomerizes unconjugated bilirubin to water soluble form

occurs after first 24 hours of life and usually resolves without treatment in 1-2 weeks

195
Q

______ are converted to bilirubin. _______ Bilirubin is bound to serum albumin and transferred to the liver where it is turned into _______ by ________. ______ is excreted into bile

A

Heme molecules (from hemoglobin)
Unconjugated (or indirect) –> water insoluble
conjugated (direct)/bilirubin diglucuronide –> water soluble
UDP-glucuronosyl transferase
Conjugated (direct) bilirubin is excreted into bile.

196
Q

All hereditary hyperbilirubinemias are ______

A

autosomal recessive

197
Q

Gilbert syndrome

A

Mild decrease in UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake

increases unconjugated bilirubin without overt hemolysis

198
Q

Crigler-Najjar syndrome, type I

A

absent UDP-glucuronosyltransferase causes increase in unconjugated bilirubin

presents early and die within few years. Need liver transplant to cure. Type II is less severe and responds to phenobarbital which increases liver enzyme synthesis

jaundice
kernicterus - bilirubin deposition in brain

199
Q

Dubin Johnson syndrome

A

conjugated hyperbilirubinemia due to defective liver excretion

grossly black dark liver

benign

200
Q

Rotor syndrome

A

similar to dubin johnson syndrome

milder and without black liver

due to impaired hepatic uptake and excretion

201
Q

Wilsons disease (hepatolenticular degeneration) is _____ inheritence and a mutation in _______. Describe the pathophys

A

autosomal recessive

mutation in hepatocyte copper transporting ATPase (ATP7B gene; chromosome 13)

decrease copper incorporation into apoceruloplasmin and excretion into bile –> drop in serum ceruloplasmin

copper accumulates in liver, brain, cornea, kidneys

202
Q

Kayser fleischer rings

A

deposits in descemet membrane of cornea in wilsons disease

203
Q

deficits in wilsons disease

A
  • neurologic
  • liver
  • psychiatric
  • kayser fleischer rings
  • hemolytic anemia
  • renal disease
204
Q

tx for wilsons disease

A

chelation with penicillamine or trientine, oral zinc

205
Q

Hemochromatosis inheritence, mutation, HLA type

A

autosomal recessive

C282Y mutation on HFE gene of chromosome 6

associated with HLA A3

206
Q

Abnormal iron sensing and increased intestinal absorption that causes iron overload. What is this disease? where does iron like to accumulate?

A

hemochromatosis

in liver, pancreas, skin, heart, pituitary, joints

iron can be identified with prussian blue stain

207
Q

Patient is 40 yo and has liver cirrhosis, diabetes mellitus, and is now complaining of increase skin pigmentation. on blood work you notice there is >20 g total body iron. What is the pt diagnosis and what else are they at risk for? What is the common cause of their death? treatment?

A

hemochromatosis

restrictive cardiomyopathy (classic) or dilated cardiomyopathy (revesible)

hypogonadism

arthropathy due to calcium pyrophosphate deposition, esp in metacarpophalangel joints

high risk of HCC death

208
Q

Treatment for hemochromatosis

A

repeated phlebotomy
chelation with deferasirox
deferoxamine
oral deferiprone

209
Q

Pt presents with pruritis, jaundice, dark urine, and light colored stool. You also notice hepatosplenomegaly. Labs show high conjugated bilirubin, cholesterol, and ALP

A

Biliary tract disease

210
Q

“onion skin” bile duct fibrosis

A

primary sclerosing cholangitis

bile duct fibrosis causes alternating strictures and dilation with beading of intra and extrahepatic bile ducts on ERCP

classically seen in middle aged men with IBD

associated with ulcerative cholitis, p-ANCA +, and high igM

211
Q

Primary biliary chilangitis

A

autoimmune reaction that causes lymphocytic infiltrate + granulomas –> destruction of lobular bile ducts

classically seen in middle aged women

anti-mitochondrial antibody + and high igM

212
Q

secondary biliary cholangitis

A

extrahepatic biliary obstruction that increases pressure in intrahepatic ducts –> injury/fibrosis and bile stasis

usually in patients with known obstructive lesions and may be complicated with ascending cholangitis

213
Q

high cholesterol, high bilirubin, low bile salts, and gallbladder stasis can cause ____? What are the main risk factors for this disease?

A

Gallstones (cholelithiasis)

80% are cholesterol stones (radiolucent unless calcified)
Can also have pigment stones (black is radiopaque and brown is radiolucent)

4 Fs- female, fat, fertile (multiparity), forty

214
Q

Biliary colic

A

pain occurs due to a gallstone temporarily blocking the bile duct.

215
Q

choledocholithiasis

A

presence of gallstones in common bile duct

elevated ALP,GGT, direct bilirubin, and or AST/ALT

216
Q

gallstone ileus

A

fistula between gallbladder and GI tract causes stone to enter GI lumen and obstruct at the ileocecal valve (narrowest point)

can see air in biliary tree (pneumobilia)

217
Q

What kind of cancer is common in the porcelain gallbladder

A

calcified gallbladder has high risk of gallbladder adenocarcinoma

have prophylactic cholecystectomy

218
Q

Charcot triad of cholangitis

A

jaundice
fever
RUQ pain

219
Q

Reynolds pentad of cholangitis

A

charcots triad of cholangitis + altered mental status and shock

jaundice
Fever
RUQ pain
altered mental status
shock (hypotension)
220
Q

acute pancreatitis

A

autodigestion of pancreas by pancreatic enzymes

on imaging the pancreas is surrounded by edema

causes:

  • idiopathic
  • gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion sting
  • Hypercalcemia/hypertriglyceridemia (>1000)
  • ERCP
  • Drugs

“I GET SMASHED”

221
Q

Diagnosis criteria for acute pancreatitis

A

2 of the 3

  • acute epigastric pain that radiates to the back
  • high serum amylase or lipase (more specific) to 3x upper limit of normal
  • characteristic imaging findings
222
Q

complications of acute pancreatitis

A 
pseudocyst lined by granulation tissue not epithelium
abscess
necrosis
hemorrhage
infection
organ failure
hypocalcemia
223
Q

Chronic pancreatitis

A

chronic inflammation, atrophy, calcification of the pancreas

caused by alcohol abuse and genetic predisposition

complicated by pancreatic insufficiency ( <10% function and may manifest with steatorrhea and fat soluble vitamin deficiency, diabetes mellitus)

and pseudo cysts (surrounded by granulation tissue not epithelium)

224
Q

Pancreatic adenocarcinoma

A

very aggressive tumor arising from pancreatic ducts (disorganized glandular structure with cellular infiltration)

often metastatic at presentation

associated with CA19-9 tumor marker and also CEA

225
Q

patients presents with weight loss, redness and tenderness on palpation of extremities, and pain that radiates to the back

A

pancreatic adenocarcinoma

weight loss is due to malabsorption and anorexia

migratory thrombophlebitis (red and tender) is trousseau syndrome

courvoisier sign

226
Q

courvoisier sign

A

obstructive jaundice with palpable, nontender gallbladder

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