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From Flashcardlet > GI First Aid > Flashcards

GI First Aid Flashcards

With Pathoma

0
Q

To what does the midgut give rise?

A

duodenum –> transverse colon

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1
Q

To what does the foregut give rise?

A

pharynx –> duodenum

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2
Q

To what does the hindgut give rise?

A

distal transverse colon –> rectum

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3
Q

What is a gastroschisis?

A

failure of lateral fold closure –> extrusion of abdominal contents through the abdominal folds; NOT covered by peritoneum

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4
Q

What is a omphalocele?

A

failure of lateral fold closure –> persistence of herniation of abdominal contents into umbilical cord; covered by peritoneum and amnion

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5
Q

Which is covered by peritoneum: gastroschisis or omphalocele?

A

omphalocele

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6
Q

If the rostral fold fails to close, what will result?

A

sternal defects

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7
Q

If the lateral fold fails to close, what will result?

A

omphalocele

gastroschisis

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8
Q

If the caudal fold fails to close, what will result?

A

bladder exstrophy

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9
Q

What causes duodenal atresia, and with what is it associated?

A

CAUSE failure to recanalize

ASSOCIATION trisomy 21

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10
Q

What causes jejunal, ileal, and colonic atresia (“apple peel atresia”)?

A

vascular accident

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11
Q

When does the midgut herniate through the umbilical ring?

A

6th week

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12
Q

When does the midgut return to the abdominal cavity AND rotate around the superior mesenteric artery?

A

10th week

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13
Q

What are the most commonly seen pathologies of embryological development of the GI system?

A

malrotation of midgut
omphalocele
intestinal atresia or stenosis
volvulus

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14
Q

What is the most common tracheoesophageal anomaly?

A

esophageal atresia with distal tracheoesophageal fistula (85%)

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15
Q

What are the signs and symptoms of esophageal atresia with distal tracheoesophageal fistula?

A

SYMPTOMS drooling, choking, vomiting with first feeding; cyanosis secondary to laryngospasm; polyhydramnios, abdominal extension, aspiration
CXR air entering stomach
TEST failure to pass nasogastric tube into stomach

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16
Q

In pure esophageal atresia, what will be seen on CXR?

A

gasless abdomen

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17
Q

What does “H-type” tracheoesophageal anomaly signify?

A

isolated TEF (tracheoesophageal fistula)

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18
Q

What causes congenital pyloric stenosis?

A

hypertrophy of pylorus –> obstruction

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19
Q

What is the epidemiology of congenital pyloric stenosis?

A

1/600 live births, more often in firstborn males

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20
Q

What are the symptoms of congenital pyloric stenosis?

A

palpable “olive” mass in epigastric region
nonbilious projective vomiting at approximately 2 weeks of age
visible peristalsis

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21
Q

What is the treatment for congenital pyloric stenosis?

A

surgical incision. myotomy

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22
Q

From where is the pancreas derived?

A

foregut:
VENTRAL PANCREATIC BUDS –> pancreatic head and main pancreatic duct
VENTRAL BUD –> uncinate process
DORSAL PANCREATIC BUD –> everything else! (body, tail, isthmus, and accessory pancreatic duct)

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23
Q

What causes an annular pancreas?

A

VENTRAL pancreatic bud abnormally encircles second part of duodenum –> ring of pancreatic tissue formed –> possible duodenal narrowing and obstruction

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24
Q

What causes pancreas divisum?

A

ventral and dorsal parts fail to fuse

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25
Q

When should the ventral and dorsal portions of the pancreas fuse?

A

8th week

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26
Q

From where does the spleen arise, and from where is it supplied?

A

ARISE mesentery of stomach (mesodermal)

SUPPLY forgut via the celiac artery

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27
Q

What are the retroperitoneal structures?

A 
Suprarenal (adrenal) gland
Aorta, IVC
Duodenum, second and third parts
Pancreas, all but tail
Ureters
Colon, descendening and ascending
Kidneys
Esophagus, lower 2/3
Rectum, lower 2/3
--SADPUCKER--
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28
Q

What may result from injuries to the retroperitoneal structures?

A

blood or gas accumulation in retroperitoneal space

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29
Q

From what is the falciform ligament derived, to where does it connect, and what structures does it contain?

A

DERIVATION ventral mesentery
CONNECTION anterior abdominal wall
CONTAINS ligamentum teres hepatis (fetal umbilical vein)

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30
Q

To what does the hepatoduodenal ligament connect, what does it itself connect, and what does it contain?

A

CONNECTION duodenum
CONNECTS greater and lesser sacs
CONTAINS portal triad (hepatic artery, portal vein, common bile duct)

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31
Q

What is the Pringle manuever?

A

compression of the hepatoduodenal ligament between the thumb and index finger in omental foramen to control bleeding

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32
Q

To what does the gastrohepatic ligament connect, what does it separate, and what does it contain?

A

CONNECTION liver to lesser curvature of stomach
SEPARATES greater and lesser sacs on the right
CONTAINS gastric arteries

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33
Q

To what does the gastrocolic ligament connect, of what is it a part, and what does it contain?

A

CONNECTION greater curvature and transverse colon
PART OF greater omentum
CONTAINS gastroepiploic arteries

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34
Q

To what does the gastrosplenic ligament connect, what does it separate, and what does it contain?

A

CONNECTION greater curvature and spleen
SEPARATES greater and lesser sacs on left
CONTAINS short gastrics, left gastroepiploic vessels

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35
Q

To what does the splenorenal ligament connect, and what does it contain?

A

CONNECTION spleen to posterior abdominal wall

CONTAINS splenic artery and vein; tail of pancreas

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36
Q

What separates the greater and lesser sacs on the right? And on the left?

A

RIGHT gastrohepatic ligament

LEFT gastrospenic ligament

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37
Q

What are the layers of the gut wall from inside to outside?

A

Mucosa (epithelium for absorption, lamina propria for support, muscularis mucosa for motility)
Submucosa (includes Submucosal nerve plexus [Meissner’s])
Muscularis externa (includes yenteric nerve plexus [Auerbach’s])
Serosa when intraperitoneal / Adventitia when retroperitoneal
–MSMS–

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38
Q

In which layer(s) is/are erosions found?

A

mucosa ONLY

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39
Q

In which layer(s) is/are ulcers found?

A

submucosa, inner or outer muscular layer

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40
Q

What is the histology of the esophagus?

A

nonkeratinized stratified squamous epithelium

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41
Q

What is the histology of the stomach?

A

gastric glands

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42
Q

What is the histology of the duodenum?

A

villi and microvilli increase absorptive surface

Brunner’s glands (submucosa) and crypts of Lieberkühn

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43
Q

What is the histology of the jejunum?

A

plicae circulares

crypts of Lieberkühn

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44
Q

What is the histology of the ileum?

A

peyer’s pathces (lamina propria, submucosa)
plicae circulares (proximal ileum)
crypts of Lieberkühn

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45
Q

What is the histology of the colon?

A

crypts BUT NO villi

numberous goblet cells

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46
Q

Which direction do arteries supplying the GI structures branch?

A

anteriorly

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47
Q

Which direction do arteries supplying non-GI structure branch?

A

laterally

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48
Q

Answer the following regarding structures derived from the foregut:

  1. Artery supply
  2. PNS innervation
  3. Vertebral level
A
  1. celiac
  2. vagus
  3. T12/L1
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49
Q

Answer the following regarding structures derived from the midgut:

  1. Artery supply
  2. PNS innervation
  3. Vertebral level
A
  1. SMA
  2. vagus
  3. L1
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50
Q

Answer the following regarding structures derived from the hindgut:

  1. Artery supply
  2. PNS innervation
  3. Vertebral level
A
  1. IMA
  2. pelvic
  3. L3
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51
Q

What are the structures arising from the foregut?

A 
proximal duodenum
liver
gallbladder
pancreas
spleen (mesoderm)
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52
Q

Answer the following regarding the proximal duodenum, liver, gallbladder, pancreas, spleen (mesoderm):

  1. Artery supply
  2. PNS innervation
  3. Vertebral level
A
  1. celiac
  2. vagus
  3. T12/L1
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53
Q

What are the structures arising from the midgut?

A

distal duodenum to proximal 2/3 of the transverse colon

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54
Q

Answer the following regarding the distal duodenum to proximal 2/3 of the transverse colon:

  1. Artery supply
  2. PNS innervation
  3. Vertebral level
A
  1. SMA
  2. vagus
  3. L1
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55
Q

What are the structures arising from the hindgut?

A

distal 1/3 of the transverse colon to upper portion of rectum
splenic fixture is a watershed region

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56
Q

Answer the following regarding the distal 1/3 of the transverse colon to the upper portion of the rectum:

  1. Artery supply
  2. PNS innervation
  3. Vertebral level
A
  1. IMA
  2. pelvic
  3. L3
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57
Q

What are the branches of the celiac trunk?

A

common hepatic
splenic
left gastric

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58
Q

What are the arteries constituting the main blood supply of the stomach?

A

common hepatic
splenic
left gastric

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59
Q

If the splenic artery is blocked, what arteries will be most at risk?

A

short gastrics due to poor anastomoses

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60
Q

What are the strong anastomoses of the stomach?

A

left and right gastroepiploics

left and right gastrics

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61
Q

What are the four collateral circulation paths that compensate for a blockage in the abdominal aorta?

A
  1. superior epigastric (from the internal thoracic / mammary) <–> inferior epigastric (from the external iliac)
  2. superior pancreaticoduodenal (celiac trunk) <–> inferior pancreaticoduodenal (SMA)
  3. middle colic (SMA) <–> left colic (IMA)
  4. superior rectal (IMA) <–> middle and inferior rectal (internal iliac)
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62
Q

What is the anastomoses at the esophagus?

A

left gastric <–> esophageal

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63
Q

What is the anastomoses at the umbilicus?

A

paraumbilical <–> superficial and inferior epigastric BELOW the umbilicus; superior epigastric and lateral thoracic ABOVE the umbilicus

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64
Q

What is the anastomoses at the rectum?

A

superior rectal <–> middle and inferior rectal

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65
Q

What are the signs of portal HTN?

A

esophageal varices
caput medusa
internal hemorrhoids

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66
Q

What is the treatment of portal HTN?

A

TIPS (transjugular intraheptaic portosystemic shunt) between the portal vein and hepatic vein percutaneously, which relieves portal HTN by shunting blood to the systemic circulation

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67
Q

Are internal hemorrhoids painful?

A

No, they receive visceral innervation

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68
Q

Are external hemorrhoids painful?

A

Yes, they receive somatic innvervation from the inferior rectal branch of the pudendal nerve

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69
Q

Where is the pectinate (dentate) line?

A

where the endodern and ectoderm meet

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70
Q

What pathologies are found above the pectinate line?

A

internal hemorrhoids

adenocarcinoma

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71
Q

What is the vascular supply above the pectinate line?

A

superior rectal artery, from the IMA

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72
Q

What is the venous and lymphatic drainage of the area above the pectinate line?

A

VENOUS superior rectal vein –> inferior mesenteric vein –> portal system
LYMPHATIC deep nodes

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73
Q

What pathologies are found below the pectinate line?

A

external hemorrhoids

squamous cell carcinoma

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74
Q

What is the vascular supply below the pectinate line?

A

inferior rectal artery, from the internal pudendal artery

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75
Q

What is the venous and lymphatic drainage of the area below the pectinate line?

A

VENOUS inferior rectal vein –> internal pudendal vein –> internal iliac vein –> IVC
LYMPHATIC superficial inguinal nodes

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76
Q

Does the basolateral surface of the hepatocytes face the sinusoids or the bile canaliculi?

A

sinusoids

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77
Q

Does the apical surface of the hepatocytes face the sinusoids or the bile canaliculi?

A

bile canaliculi

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78
Q

Which area of the liver is affected first by viral hepatitis?

A

Zone I, periportal zone

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79
Q

Which area of the liver is affected first by ischemia?

A

Zone III, the pericentral vein (centrilobular zone)

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80
Q

Which area of the liver is the site of alcoholic hepatitis?

A

Zone III, the pericentral vein (centrilobular zone)

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81
Q

Which area of the liver contains the P450 system?

A

Zone III, the pericentral vein (centrilobular zone)

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82
Q

Which area of the liver most sensitive to toxic injury?

A

Zone III, the pericentral vein (centrilobular zone)

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83
Q

If gallstones reach the ampulla of Vater, what ducts will be blocked (if any)?

A

BOTH the bile and pancreatic ducts

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84
Q

Obstruction of the common bile duct can result from a tumor arising where?

A

head of the pancreas, near the duodenum

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85
Q

What is the organization of the femoral region?

A

lateral to medial: nerve-artery-vein-empty space-lympatics

–NAVEL–

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86
Q

What occurs in the femoral triangle?

A

femoral vein, artery, and nerve

–Venous near the penis–

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87
Q

Where is the femoral sheath, and what does it contain?

A

DEFINITION fascial tube 3-4 cm below the inguinal ligament

CONTAINS femoral vein, artery and canal (deep inguinal lymph nodes) but NOT the femoral nerve

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88
Q

From where does the internal spermatic fascia arise?

A

transversalis fascia

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89
Q

From where does the cremasteric muscle and fascia arise?

A

internal oblique

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90
Q

From where does the external spermatic fascia arise?

A

external oblique

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91
Q

What happens in a diaphragmatic hernia?

A

abdominal structures enter the thorax, may occur in infants as a result of defective development of pleuroperitoneal membrane

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92
Q

What is a hiatal hernia?

A

stomach herniates upward through the esophageal hiatus in the diaphragm

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93
Q

What is a sliding hiatal hernia?

A

GE junction is displaced upward, causing an hourglass stomach

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94
Q

What is a paraesophageal hernia?

A

GE junction is normal; fundus protrudes into thorax

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95
Q

What is an indirect inguinal hernia?

A

goes through the internal (deep) inguinal ring (lateral to the inferior epigastric artery), external (superficial) inguinal ring, and into the scrotum
occurs in infants due to the failure of processus vaginalis to close (can form a hydrocele)

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96
Q

In what sex is an indirect inguinal hernia more common?

A

males; follows the path of the descent of the testes and is thus covered by all 3 layers of the spermatic fascia

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97
Q

What is a direct inguinal hernia?

A

protrudes through the inguinal (Hesselbach’s) triangle, belgues directly through the abdominal wall medial to the inferior epigastric artery.
goes through the EXTERNAL (superficial) inguinal ring ONLY; covered by external spermatic fascia

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98
Q

In what group are direct inguinal hernias most commonly seen?

A

older males

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99
Q

Which type of hernia is medial to the inferior epigastric artery? Which is lateral?

A

MEDIAL direct
LATERAL indirect
–MDs don’t LIe–

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100
Q

What is a femoral hernia?

A

protrudes below inguinal ligament through femoral canal below and lateral to the pubic tubercle

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101
Q

In what sex are femoral hernias most commonly seen?

A

women

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102
Q

What is the leading cause of bowel incarceration?

A

femoral hernias

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103
Q

What is the most common type of hernia?

A

sliding hiatal hernia

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104
Q

What is Hesselbach’s triangle?

A

inferior epigastric vessels
lateral border of rectus abdominis
inguinal ligament

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105
Q

From where is gastrin secreted?

A

G cells in the antrum of the stomach

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106
Q

What are the effects of gastrin?

A

increased gastric H+ secretion, growth of gastric mucosa, and gastric motility

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107
Q

How is gastrin regulated?

A

INCREASED stomach distention and alkalinization, amino acids, peptides, vagal stimulation
DECREASED stomach pH < 1.5

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108
Q

What two amino acids are potent stimulators of gastrin?

A

phenylalanine, tryptophan

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109
Q

In what two issues are gastrin release increased?

A

greatly increased in Zollinger-Ellison syndrome

increased in chronic PPI use

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110
Q

From where is cholecystokinin released?

A

I cells in the duodenum and jejunum

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111
Q

What are the effects of cholecystokinin?

A

INCREASED pancreatic secretion (via neural muscarinic pathways), gallbladder contraction, and relaxation of the sphincter of Oddi
DECREASED gastric emptying

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112
Q

How is cholecystokinin regulated?

A

INCREASED fatty acids, amino acids

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113
Q

By what method does cholecystokinin affect the pancreas?

A

acts on neural muscarinic pathways –> increased pancreatic secretion

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114
Q

From where is secretin released?

A

S cells of the duodenum

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115
Q

What are the effects of secretin?

A

INCREASED pancreatic HCO3- secretion, bile secretion

DECREASED gastric acid secretion

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116
Q

What regulates release of secretin?

A

INCREASED BY acids, fatty acids in lumen of duodenum

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117
Q

How does secretin influence pancreatic enzyme efficacy?

A

increased secretion –> increased HCO3- –> increased neutralization of gastric acid in the duodenum –> pancreatic enzymes allowed to function

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118
Q

From where is somatostatin released?

A

D cells of the pancreatic islets and GI mucosa

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119
Q

What are the effects of somatostatin?

A

DECREASED gastric acid and pepsinogen secretion, pancreatic and small intestine fluid secretion, gallbladder contraction, insulin and glucagon release

Antigrowth hormone effects as it inhibits digestion and absorption of substances needed for growth.

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120
Q

How is somatostatin regulated?

A

INCREASED BY acid

DECREASED BY vagal stimulation

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121
Q

From where is gastric inhibitory peptide / glucose-dependent insulinotropic peptide?

A

K cells of the duodenum and jejunum

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122
Q

What is the exocrine effect of gastric inhibitory peptide / glucose-dependent insulinotropic peptide?

A

DECREASED gastric H+ secretion

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123
Q

What is the endocrine effect of gastric inhibitory peptide / glucose-dependent insulinotropic peptide?

A

INCREASED insulin release

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124
Q

How is gastric inhibitory peptide / glucose-dependent insulinotropic peptide regulated?

A

INCREASED BY fatty acids, amino acids, oral glucose

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125
Q

From where is vasoactive intestinal polypeptide (VIP) released?

A

parasympathetic ganglia in sphincters, gallbladder, small intestine

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126
Q

What are the effects of vasoactive intestinal polypeptide (VIP)?

A

INCREASED intestinal water and electrolyte secretion, relaxation of intestinal smooth muscle and sphincters

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127
Q

How is vasoactive intestinal polypeptide (VIP) regulated?

A

INCREASED BY distention and vagal stimulation

DECREASED BY adrenergic input

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128
Q

What is a VIPoma?

A

non-alpha, non-beta islet cell pancreatic tumor that secretes VIP, copious Watery Diarrhea, Hypokalemia, and Achlorhydria
–WDHA syndrome–

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129
Q

What are the affects of nitric oxide?

A

INCREASED smooth muscle relaxation, including LES

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130
Q

In what is the loss of NO secretion implicated?

A

increased LES tone in achalasia

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131
Q

From where is motilin released?

A

small intestine

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132
Q

What is the affect of motilin?

A

produces migrating motor complexes (MMCs)

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133
Q

How is motilin regulated?

A

INCREASED IN fasting state

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134
Q

How is motilin associated with peristalsis?

A

motilin receptor agonists, such as erythromycin, are used to stimulate intestinal peristalsis

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135
Q

From where is intrinsic factor released?

A

parietal cells of the stomach

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136
Q

What is the action of intrinsic factor?

A

vitamin B12-binding protein, required for B12 uptake in the terminal ileum

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137
Q

What is the result of autoimmune destruction of parietal cells?

A

chronic gastritis and pernicious anemia

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138
Q

From where is gastric acid secreted?

A

parietal cells of the stomach

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139
Q

What is the effect of gastric acid secretion?

A

DECREASED stomach pH

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140
Q

How is gastric acid regulated?

A

INCREASED BY histamin, ACh, gastrin

DECREASED BY somatostatin, GIP, prostaglandin, secretin

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141
Q

What is a gastrinoma?

A

gastrin-secreting tumor –> continuous high levels of acid secretion, ulcers

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142
Q

From where is pepsin secreted?

A

chief cells of the stomach

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143
Q

What is the action of pepsin?

A

protein digestion

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144
Q

How is pepsin regulated?

A

INCREASED BY vagal stimulation, local acid

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145
Q

From where is HCO3- released?

A

mucosal cells (stomach, duodenum, salivary glands, pancrease) and Brunner’s glands (duodenum)

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146
Q

What is the effect of HCO3- in the stomach?

A

neutralizes acid

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147
Q

How is HCO3- regulated?

A

INCREASED BY pancreatic and biliary secretion with secretin

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148
Q

Where is HCO3- trapped?

A

mucus that covers the gastric epithelium

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149
Q

From where is saliva secreted?

A

parotid, submandibular, sublingual glands, stimulated by sympathetic and parasympathetic activity

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150
Q

What does amylase digest?

A

starch

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151
Q

Is saliva normally hypotonic, isotonic, or hypertonic?

A

hypotnoic because of absorption, but more isotonic with higher flow rates (less time for absorption)

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152
Q

What effect does atropine have in the stomach?

A

blocks vagal stimulation of parietal cells

vagal stimulation of G cells is unaffected, as a different transmitter is used (GRP)

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153
Q

Does gastrin increase acid secretion primarily by ECL cell effects or direct effect on parietal cells?

A

effect on ECL cells –> histamine release

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154
Q

Where are Brunner’s glands located, what are their effects, and in what pathology are they indicated?

A

LOCATION duodenal submucosa
EFFECT secretion of alkaline mucus
PATHOLOGY hypertrophy in peptic ulcer disease

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155
Q

Are pancreatic secretions hypotonic, isotonic, or hypertonic?

A

isotonic

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156
Q

What are the pancreatic secretions?

A

alpha-amylase
lipase, phospholipase A, colipase
proteases
trypsinogen

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157
Q

When pancreatic secretions are at a low flow rate, does Cl- or HCO3- predominate?

A

Cl-

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158
Q

When pancreatic secretions are at a high flow rate, does Cl- or HCO3- predominate?

A

HCO3-

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159
Q

What is the role of alpha-amylase?

A

digestion of starches

NOTE secreted in active form

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160
Q

What is the role of lipase, phospholipase A, and colipase?

A

fat digestion

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161
Q

What is the role of proteases, and what enzymes are included in that group?

A

ROLE protein degradation
TYPES trypsin, chymotrypsin, elastase, carboxypeptidases

NOTE secreted in proenzyme form of zymogen

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162
Q

What enzyme converts trypsinogen to trypsin, and from where is it secreted?

A

ENZYME enterokinase/enteropeptidase

FROM duodenal mucosa

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163
Q

What is the effect of trypsin?

A

activation of other proenzymes; positive feedback loop in the creation of trypsinogen

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164
Q

What biochemical effect does salivary amylase?

A

hydrolysis of alpha-1,4 linkages –> disaccharides (maltose and alpha-limit dextrins)

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165
Q

What is the biochemical effect of pancreatic amylase?

A

hydrolysis of starch –> oligosaccharides, disaccharides

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166
Q

Where is the concentration of pancreatic amylase highest?

A

duodenal lumen

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167
Q

What is the rate-limiting step in carbohydrate digestion?

A

oligosaccharide hydrolases

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168
Q

Where do oligosaccharide hydrolases act?

A

brush border of the intestine

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169
Q

What is the biochemical effect of oligosaccharide hydrolases?

A

oligosaccharides, disaccharides –> monosaccharides

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170
Q

Upon which gastric parietal cell receptor does ACh act?

A

M3

NOTE this action is blocked by atropine

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171
Q

Upon which gastric parietal cell receptor does gastrin act?

A

CCKb

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172
Q

Upon which gastric parietal cell receptor does histamine act?

A

H2

NOTE this action is blocked by cimetidine, ranitidine, famotidine, nizatidine

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173
Q

What is the most important mechanism regulating the interaction of gastrin and the CCKb receptor?

A

ECL cells

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174
Q

Acting through Gi, what factors inhibit cAMP within the gastric parietal cell, thus removing the stimulation of the H+/K+ ATPase (proton pump)?

A

prostaglandins and misoprostol through one receptor

somastostatin through another receptor

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175
Q

What enzyme stimulates the reversible reaction between CO2 + H2O and H2CO3?

A

carbonic anhydrase

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176
Q

What form of carbohydrates can enterocytes absorbed?

A

monosaccharides (glucose, galactose, fructose)

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177
Q

Which receptor brings glucose and galactose into an enterocyte?

A

SGLT1 (Na+ dependent)

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178
Q

Which receptor brings fructose into an enterocyte?

A

GLUT-5 (facilitated diffusion)

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179
Q

How are carbohydrates transported to the blood from enterocytes?

A

GLUT-2

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180
Q

What is the use of a D-xylose absorption test?

A

distinguishes GI mucosa damage from other causes of malabsorption

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181
Q

How is iron absorbed in the GI tract?

A

as Fe2+ through DMT-1 in the duodenum

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182
Q

What secretes hepcidin?

A

hepatocytes

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183
Q

Where is folate absorbed?

A

jejunum

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184
Q

How and where is B12 absorbed in the GI tract?

A

requires intrinsic factor; absorbed with bile acids in the terminal ileum

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185
Q

What is the histological appearance of Peyer’s patches?

A

unencapsulated lymphoid tissue found in the lamina propria and submucosa of the ileum; contain specialized M cells that take up antigen

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186
Q

With what immunoglobulin are Peyer’s patches associated and why?

A

IgA
B cell stimulation in Peyer’s patches –> B cell differentiation into IgA-secreting plasma cells (lamina propria) –> IgA receives protective secretory component –> transportation across epithelium to gut –> encounters intraluminal antigen

–SECRETORY IgA, the Intra-Gut Antibody”

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187
Q

What is the composition of bile?

A 
bile salts (bile acids conjugated to glycine or taurine, thus making them WATER SOLUBLE)
phospholipids
cholesterol
bilirubin
water
ions
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188
Q

Are bile salts water soluble or insoluble?

A

soluble: they are conjugated to glycine or taurine

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189
Q

What enzyme catalyzes the rate-limiting step of bile formation?

A

cholesterol 7-alpha-hydroxylase

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190
Q

What are the three functions of bile?

A
  1. digestion and absorption of lipids and fat-soluble vitamins
  2. cholesterol excretion (body’s ONLY means of eliminating cholesterol)
  3. membrane disruption –> antimicrobial activity
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191
Q

Where are RBCs broken down into heme, then unconjugated bilirubin?

A

macrophages

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192
Q

Where does unconjugated bilirubin complex with albumin?

A

bloodstream

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193
Q

Where does unconjugated bilirubin become conjugated bilirubin, and what enzyme catalyzes this step?

A

liver

UDP-glucuronosyl transferase

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194
Q

From what are urobilin and stercobilin derived?

A

urobilinogen

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195
Q

What percentage of urobilinogen is excreted in the feces as stercobilinogen?

A

80%

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196
Q

What percentage of urobilinogen is excreted in the urine as urobilin?

A

2%

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197
Q

What percentage of urobilinogen reenters the liver via enterohepatic circulation?

A

18%

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198
Q

With what is bilirubin conjugated?

A

glucuronic acid

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199
Q

What type of glands are salivary glands?

A

exocrine, secrete saliva

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200
Q

What are the major and minor salivary glands?

A

MAJOR parotid, submandibular, sublingual

MINOR hundreds of microscopic glands distributed throughout the oral mucosa

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201
Q

What si the presentation of mumps?

A

SYMPTOMS bilateral inflamed parotid glands, orchitis, pancreatitis, aseptic meningitis
LABS increased serum amylase

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202
Q

What is sialadenitis, and what is its most common cause?

A

DEFINITION unilateral inflammation of the salivary gland due to S. aureus
CAUSES obstructing stone (sialolithiasis)

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203
Q

In which gland do the majority of salivary gland tumors arise?

A

parotid gland

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204
Q

What is the most common salivary gland tumor?

A

pleomorphic adenoma

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205
Q

What is the second most common tumor of the salivary glands?

A

Warthin’s tumor (papillary cystadenoma lymphomatosum)

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206
Q

What is the most common malignant tumor of the salivary glands?

A

mucoepidermoid carcinoma

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207
Q

What is the presentation of a pleomorphic adenoma?

A

DEFINITION benign mixed tumor of stromal and epithelial tissue
PRESENTATION mobile, painless, circumscribed mass at the angle of the jaw

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208
Q

Is there a high rate of recurrence in pleomorphic adenomas? Why or why not?

A

yes

extension of small islands of tumor through tumor capsule leads to incomplete resection

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209
Q

If a pleomorphic adenoma transforms into carcinoma, what sign may result?

A

facial nerve damage as the facial nerve runs through the parotid gland

NOTE transformation to carcinoma is rare

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210
Q

What is Warthin’s tumor?

A

papillary cystadenoma lymphomatosum, a benign cystic tumor with abundant lymphocytes and germinal centers (lymph-node like stroma) arising in the parotid

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211
Q

What is a mucoepidermoid carcinoma?

A

malignant tumor composed of mucinous and squamous cells, usually arising in the parotid and involving the facial nerve (thus presenting painfully)

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212
Q

What is an esophageal web, what is its histology, and how does it present?

A

DEFINITION thin protrusion of esophageal mucosa, most often in the anterior wall of the upper esophagus
HISTOLOGY stratified squamous epithelium
PRESENTATION dysphagia for poorly chewed food, Plummer-Vinson syndrome (5% of cases are asymptomatic)

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213
Q

What is the major complication of an esophageal web?

A

increased risk for esophageal squamous cell carcinoma

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214
Q

What is Plummer-Vinson syndrome?

A

severe iron deficiency anemia
dysphagia due to esophageal web
beefy-red tongue (atrophic glossitis)

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215
Q

What is Zenker diverticulum, and how does it present?

A

DEFINITION outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum), arising immediately above the UES at the junction of the esophagus and pharynx
PRESENTATION dysphagia and regurgitation, obstruction, halitosis due to presence of undigested food in esophagus, chest discomfort, weight loss

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216
Q

How is Zenker diverticulum treated?

A

myotomy if large
endoscopy clip
botulinum toxin

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217
Q

What is BoerHaave Syndrome, and with what is it associated?

A

DEFINITION transmural esophageal RUPTURE due to violent retching –> air in the mediastinum, subcutaneous emphysema causing sternal and/or supraclavicular crepitis; YOU WILL HEAR CRACKLES
ASSOCIATION Mallory-Weiss syndrome
–Been Heaving Syndrome–

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218
Q

With what is esophagitis associated?

A

reflux
infection (Candida, HSV-1, or CMV)
chemical ingestion

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219
Q

What is the most common sign of Candida esophagitis?

A

white pseudomembrane on the tongue

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220
Q

What is seen on microscopy in esophagitis due to HSV-1?

A

punched out ulcers

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221
Q

What is seen on microscopy in esophagitis due to CMV?

A

linear ulcers

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222
Q

With what are esophageal strictures associated?

A

lye ingestion

acid reflux

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223
Q

What is Mallory-Weiss syndrome and how does it present?

A

DEFINITION alcholism, bulimia –> severe vomiting –> longitudinal laceration of mucosa at the gastroesophageal junction
PRESENTATION painful hematemesis

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224
Q

What is the pathogenesis of esophageal varices?

A

portal HTN –> portal vein cannot drain into the left gastric vein –> left gastric vein backs up into the esophageal vein –> dilation of the submucosal veins of the lower 1/3 of the esophagus

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225
Q

What is the presentation and complication of esophageal varices?

A

PRESENTATION usually asymptomatic, but may present with painless hematemesis
COMPLICATION rupture –> death

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226
Q

What is the most common cause of death in cirrhosis?

A

rupture of esophageal varices

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227
Q

What increases the risk of psuedodiverticulum?

A 
inflammation
fibrosis
GERD
chronic Candidiasis
caustic ingestion
malignancy
strictures
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228
Q

In what population is psuedodiverticulum most commonly seen?

A

men, 6th-7th decades

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229
Q

What is the pathogenesis of achalasia?

A

ganglion cells of the myenteric (Aeurbach’s) plexus OR vagus nerve undergo degeneration –> failure of relaxation of LES –> high LES opening pressure and uncoordinated peristalsis –> progressive dysphagia to solids and liquids

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230
Q

Which presents with dysphagia to solid foods only?

Obstruction or achalasia.

A

obstruction

231
Q

Which presents with dysphagia to both solids and liquids?

Obstruction or achalasia.

A

Achalasia

232
Q

What infectious agent is associated with achalasia?

A

Trypanosoma cruzi in Chagas disease

233
Q

What is the presentation of achalasia?

A

dysphagia for solids and liquids
putrid breath
high LES pressure on esophageal manometry
“bird-beak” sign on barium swallow study
increased risk for esophageal squamous cell carcinoma

234
Q

What systemic illness is associated with achalasia? What test is most specific for this?

A 
ILLNESS scleroderma (CREST syndrome)
TEST anticentromeric antibody

NOTE diffuse scleroderma is best tested by anti-DNA topoisomerase I antibody

235
Q

What is the presentation of GERD?

A

heartburn, regurgitation while supine
nocturnal cough, dyspnea, adult-onset asthma
damage to tooth enamel
weight loss, bleeding

LATE COMPLICATIONS ulceration with stricture, Barrett esophagus

236
Q

What is the pathogenesis of GERD?

A

decrease in LES tone –> reflux of acid into the stomach

237
Q

What are the risk factors of GERD?

A 
alcohol
tobacco
obesity
fat-rich diet
caffeine
hiatal hernai
pregnancy
scleroderma
238
Q

How do you diagnose GERD?

A 
barium swallow
pH scope
endoscopy
biopsy
PPI trial
239
Q

What is the pathogenesis of Barrett esophagus?

A

chronic acid reflux (GERD) –> stress to lower esophageal stem cells –> replacement of nonkeratinized (stratified) squamous epithelium with intestinal (nonciliated columnar with goblet cells) epithelium in the distal esophagus –> glandular metaplasia

240
Q

With what is Barrett esophagus associated?

A

esophagitis
esophageal ulcers
increased risk of esophageal adenocarcinoma

241
Q

How common is it for GERD patients to develop Barrett esophagus?

A

10% of GERD patients progress to Barrett esophagus

242
Q

What is seen histologically in Barrett esophagus?

A

metaplastic columnar epithelium with goblet cells

243
Q

What are the types of esophageal cancer?

A

squamous cell carcinoma

adenocarcinoma

244
Q

What is the presentation of esophageal cancer?

A

progressive dysphagia (first solids, then liquids)
weight loss
pain
hematemesis
SQUAMOUS may also present with hoarseness duet o recurrent laryngeal nerve involvement and cough due to tracheal involvement

245
Q

What is the most common form of esophageal cancer in the West?

A

adenocarcinoma

246
Q

What is the most common form of esophageal cancer worldwide?

A

squamous cell carcinoma

247
Q

From what does adenocarcinoma arise?

A

Barrett esophagus, usually involves the lower 1/3 of the esophagus

248
Q

Which is more common in the Black population?

Adenocarcinoma or squamous cell carcinoma.

A

squamous cell carcinoma

249
Q

Which is more common in the Caucasian population?

Adenocarcinoma or squamous cell carcinoma.

A

adenocarcinoma

250
Q

What cytogenetic finding is associated with adenocarcinoma of the esophagus?

A

p53

251
Q

What cytogenetic finding is associated with squamous cell carcinoma of the esophagus?

A

p53

p16/INK4a

252
Q

Where in the esophagus is squamous cell carcinoma seen?

A

upper or middle 1/3

253
Q

What are the risk factors of squamous cell caricnoma of the esophagus?

A 
alcohol, tobacco
very hot tea
achalasia
esophageal web (Plummer-Vinson syndrome)
esophageal injury (lye ingestion, etc)
254
Q

Cancer in the upper 1/3 of the esophagus spreads to which lymph nodes?

A

cervical

255
Q

Cancer in the middle 1/3 of the esophagus spreads to which lymph nodes?

A

mediastinal or tracheobronchal

256
Q

Cancer in the lower 1/3 of the esophagus spreads to which lymph nodes?

A

celiac or gastric

257
Q

What are the risk factors for both types of esophageal cancer?

A 
Achalasia
Alcohol (squamous)
Barrett's esophagus (adenocarcinoma)
Cigarettes
Diverticula, Zenker's (squamous)
Esophageal web (squamous)
Familial
Fat (adenocarcinoma)
GERD (adenocarcinoma)
Hot liquids (squamous)

–AABCDEFFGH–

258
Q

What is the infectious agent causing bloody diarrhea?

comma- or s-shaped organisms, growth at 42 degrees; diagnose by stool culture

A

Campylobacter

259
Q

What is the infectious agent causing bloody diarrhea?

lactose negative, flagellar motility, animal reservoir (especially poultry and eggs); diagnose by stool culture

A

Salmonella

260
Q

What is the infectious agent causing bloody diarrhea?

lactose negative, very low ID50, produces Shiga toxin (human reservoir only); may cause HUS

A

Shigella

261
Q

What is the infectious agent causing bloody diarrhea?

0157:H7, can cause HUS; makes Shiga-like toxin

A

EHEC

262
Q

What is the infectious agent causing bloody diarrhea?

invades colonic mucosa

A

enteroinvasive E. coli

263
Q

What is the infectious agent causing bloody diarrhea?

daycare outbreaks, pseudoappendicitis; diagnose by stool culture

A

Yersinia enterocolitica

264
Q

What is the infectious agent causing bloody diarrhea?

protozoan; flask-shaped ulcer

A

Entamoeba histolytica

265
Q

What is the infectious agent causing watery diarrhea?

Traveler’s diarrhea, producing ST and LT toxins

A

Enterotoxigenic E. coli

266
Q

What is the infectious agent causing watery diarrhea?

comma-shaped organisms, rice-water diarrhea due to preformed enterotoxin

A

Vibrio cholerae

267
Q

What is the infectious agent causing bloody or watery diarrhea?
psuedomembranous colitis, seen after immunosuppression; diagnose by toxin stool culture

A

Clostridium dificile

268
Q

What is the infectious agent causing watery diarrhea?

gas gangrene

A

Clostridium perfringens

269
Q

What are the two possible infectious agents causing watery diarrhea?
protozoa

A

Giardia lamblia

Cryptosporidium

270
Q

What is the infectious agent causing watery diarrhea?

organisms seen at surface of endothelial apical membrane

A

Cryptosporidium

271
Q

What is the infectious agent causing watery diarrhea?

viral in child

A

rotavirus

272
Q

What is the infectious agent causing watery diarrhea?

viral in adult

A

norovirus

273
Q

What are the malabsorption syndromes?

A 
Tropical sprue
Whipple's disease
Celiac sprue
Disaccharidase deficiency
Abetalipoproteinemia
Pancreatic insufficiency
--These Will Cause Devastating Absorption Problems.--
274
Q

What is the general presentation of malabsorption syndromes?

A 
dirrhea
steatorrhea
weight loss
weakness
vitamin and mineral deficiencies
275
Q

What area of the small bowel does tropical sprue affect? And celiac sprue?

A

TROPICAL distal

CELIAC proximal, including duodenum

276
Q

How does tropical sprue differ from celiac disease?

A

occurs in tropical regions
arises after infectious diarrhea, responds to antibiotics
damage most prominent in jejunum and ileum; secondary vitamin B12 or folate deficiency may ensue

277
Q

What infectious agent causes Whipple’s disease, and what will be seen upon microscopy?

A

AGENT Tropheryma whippelii (gram positive)
LM PAS-positive foamy macrophages in intestinal lamina propria, mesenteric nodes (note that this appearance is similar to intestinal TB)

278
Q

What is the pathogenesis of Whipple’s disease?

A

macrophages of the small bowel lamina properia engulf T. whippelii –> chylomicrons cannot be transferred from enterocytes to lymphatics –> fat malabsorption and steatorrhea

279
Q

What are the symptoms of Whipple’s disease, which normally presents in older males?

A

Cardiac symptoms (valve involvement)
Arthralgias (synovial involvement)
Neurologic symptoms (CNS involvement)
–Foamy Whipped cream in a CAN–

280
Q

What cytogenetic findings are seen in celiac disease?

A

HLA-DQ2

DQ8

281
Q

What is the pathogenesis of celiac disease?

A

gliadin in gluten absorbed in small bowel –> deamidation by tissue transgluatminase (tTG) –> deamidated gliadin presented by APCs via MHC class II –> IL-15 –> accumulation of activated CD8+ T cells of NKG2D –> helper T cells mediate tissue damage to villi bearing MIC-A

282
Q

What is the presentation of celiac disease?

A

30-60 years: chronic diarrhea, bloating, anemia, chronic fatigue
children: abdominal distension, diarrhea, failure to thrive

dermatitis herpetiformis: small, herpes-like vesicles on skin due to IgA deposition at tips of dermal papillae

283
Q

What are the laboratory findings in celiac disease?

A

IgA antibodies against endomysium, tTG, or gliadin
IgG antibodies
duodenal biopsy: flattening of villi, hyperplasia of crypts, increased intraepithelial CD8+ lymphocytes

284
Q

What is the treatment of celiac disease?

A

gluten-free diet

NOTE small bowel carcinoma and T-cell lymphoma are late complications of refractory celiac disease

285
Q

What is the most common form of disaccharidase deficiency?

A

lactase deficiency –> lactose/milk intolerance

286
Q

What is the pathogenesis of lactose deficiency?

A

decreased function of lactase enzyme, found in the brush border of enterocytes –> osmotic diarrhea –> abdominal distension and diarrhea upon consumption of milk products

287
Q

Where is lactase normally found, and what is its purpose?

A

LOCATION tips of intestinal villi

FUNCTION lactose –> galactose + glucose

288
Q

If lactose deficiency is congenital, how is it inherited?

A

autosomal recessive, rare

289
Q

What might cause a temporary lactose deficiency?

A

small bowel infection, such as viral diarrhea

290
Q

When is a lactose tolerance tests positive for lactase deficiency?

A

administration of lactose produces symptoms
AND
glucose rises < 20 mg/dL

291
Q

In abetalipoproteinemia, which apolipoproteins are missing? How is this issue inherited?

A

B-48 and B-100

autosomal recessive

292
Q

What is the pathogenesis of abetalipoproteinemia?

A

decreased synthesis of apolipoprotein B –> inability to generate chylomicrons –> decreased secretion of cholesterol, VLDL into bloodstream –> fat accumulation in enterocytes

293
Q

What are the symptoms of abetalipoproteinemia?

A

lack of B-48 –> defective chylomicron formation –> malabsorption
deficiency of B-100 –> absent plasma VLDL, LDL

294
Q

What are the causes and presentation of pancreatic insufficiency?

A

CAUSES cystic fibrosis, obstructing cancer, chronic pancreatitis
PRESENTATION malabsorption of fat, fat-soluble vitamins (A, D, E, K) –> increased neural fat in stool

295
Q

What is the pathogenesis of acute gastritis?

A

imabalance between mucosal defenses and acidic environment –> acid damage to stomach mucosa –> superficial inflammation, erosion (loss of superficial epithelium), ulceration (loss of mucosal layer)

296
Q

What are the mucosal defenses of the stomach?

A

mucin layer produced by foveolar cells
bicarbonate secretions by surface epithelium
normal blood supply, providing nutrients and absorbing leaked acid

297
Q

What are the risk factors for acute gastritis?

A

severe burn (curling ulcer) –> hypovolemia l–> decreased blood supply –> sloughing of gastric mucosa
NSAIDS –> decreased PGE2
heavy alcohol consumption
chemotherapy
uremia
increased intracranial pressure (Cushing ulcer) –> increased stimulation of vagus nerve –> increased ACh –> increased acid production
shock –> multiple (stress) ulcers in ICU patients

–Burned by the CURLING iron; always CUSHION the Brain.–

298
Q

What is the pathogenesis of chronic gastritis, Type A?

A

antibodies against parietal cells and/or intrinsic factor –> autoimmune destruction of gastric parietal cells, located in body and fundus –> chronic inflammation of stomach mucosa

299
Q

What are the symptoms of chronic gastritis, Type A?

A

Atrophy of mucosa with intestinal metaplasia
Achlorhydria with increased gastrin levels and Antral G-cell hyperplasia
megaloblastic/pernicious Anemia due to lack of intrinsic factor
increased risk for gastric Adenocarcinoma (intestinal type)
–pernicious Anemia affects gastric Body–

300
Q

What is the pathogenesis of chronic gastritis, Type B?

A

H. pylori ureases and proteases + inflammation –> weakening of mucosal defenses of the antrum –> chronic inflammation of stomach mucosa

301
Q

What are the symptoms of chronic gastritis, Type B?

A 
epigastric abdominal pain
increased risk for ulceration (peptic ulcer disease)
gastric adenocarcinoma (intestinal type)
MALT lymphoma
--H. pylori Bacterium affects Antrum--
302
Q

Which is the most common form of chronic gastritis?

A

Type B, caused by H. pylori

303
Q

What effect does triple therapy have upon chronic gastritis, Type B, and what tests confirm eradication of H. pylori?

A

EFFECTS resolves gastritis/ulcer and reverses intestinal metaplasia
TESTS negative urea breath tests; lack of stool antigen

304
Q

What is the appearance and significance of Ménétrier’s disease?

A

APPEARANCE gastric hypertrophy with protien loss, parietal cell atrophy, increased mucous cells; rugae of stomach are so hypertrophied they look like brain gyri
SIGNIFICANCE precancerous change

305
Q

What is the presentation of general gastric carcinoma?

A 
late presentation
weight loss
abdominal pain
anemai
early satiety
RARELY as acanthosis nigricans or Leser-Trélat sign
306
Q

What is a Leser-Trélat sign?

A

explosive onset of multiple seborrheic keratoses often with an inflammatory base; can be an ominous sign of internal malignancy as part of a paraneoplastic syndrome.
In addition to the development of new lesions, preexisting ones frequently increase in size and become symptomatic.

307
Q

What are the risk factors for intestinal type gastric carcinoma?

A

intestinal metaplasia due to H. pylori and autoimmune gastritis
nitrosamines in smoked foods, as seen in Japan
blood type A
achlorhydia

308
Q

What is the histological appearance of intestinal type of gastric carcinoma?

A

large, irregular ulcer with heaped up margins
most commonly involves the lesser curvature of the antrum (similar to gastric ulcer)
gland-like, tubular

309
Q

What is the histological appearance of diffuse type of gastric carcinoma?

A

signet-ring cells, diffusely infiltrating the gastric wall
linitis plastica: desmoplasia –> thickened, leathery appearance of stomach wall
not glandular
poorly-differentiated

310
Q

Which type of gastric carcinoma carries a poor prognosis?

A

diffuse type

311
Q

Which type of gastric carcinoma is more common?

A

intestinal type

312
Q

What are the three signs of metastases from gastric carcinoma?

A

VIRCHOW’S NODE involvement of left supraclavicular node
KRUKENBERG’S TUMOR bilateral metastases to ovaries, abundant mucus, signet ring cells; seen in diffuse type
SISTER MARY JOSEPH’S NODULE subcutaneous periumbilical metastasis; seen in intestinal type

May also metastasize to liver.

313
Q

In what area of the GI tract is it more common to see peptic ulcer disease?

A

duodenum, 90% of cases

314
Q

What is the pathogenesis of a duodenal ulcer?

A

H. pylori (or less commonly, Zollinger-Ellison syndrome) –> decreased mucosal protection against gastric acid (or increased gastric acid secretion) –> ulceration –> epigastric pain improving with meals

315
Q

What is seen upon endoscopic biopsy of a duodenal ulcer?

A

hypertrophy of Brunner glands

316
Q

What is the pathogenesis of a gastric ulcer?

A

H. pylori (75%) or NSAID use, bile reflux –> decreased mucosal protection against gastric acid –> ulceration on lesser curvature of the antrum –> epigastric pain worsening with meals

INCREASED RISK of carcinoma; always check healing of a patient’s gastric ulcer

317
Q

Duodenal or gastric ulcer?

epigastric pain worsens with meals

A

gastric

318
Q

Duodenal or gastric ulcer?

epigastric pain improving with meals

A

duodenal

319
Q

What is the appearance of a benign gastric ulcer?

A

small (<3 cm), sharply demarcated (“punched-out”), surrounded by radiating folds of mucosa

320
Q

What is the appearance of a malignant gastric ulcer?

A

large, irregular with heaped up margins

321
Q

What are the possible treatments for peptic ulcer disease?

A 
antacids
anticholinergics
cimetidine
misoprostal
sucralfate
PPIs
clarithromycin
322
Q

Which type of ulcer is more likely to perforate?

A

duodenal (anterior > posterior)

323
Q

Which type of ulcer is more likely to undergo hemorrhage?

A

gastric, duodenal (posterior > anterior)

324
Q

If an ulcer on the posterior wall of the duodenum hemorrhages, which artery is bleeding?

A

gastroduodenal

325
Q

If an ulcer on the lesser curvature of the stomach hemorrhages, which artery is bleeding

A

left gastric

326
Q

Crohn’s disease or ulcerative colitis?

diordered response to intestinal bacteria

A

Crohn’s disease

327
Q

Crohn’s disease or ulcerative colitis?

younger patients

A

Crohn’s disease

328
Q

Crohn’s disease or ulcerative colitis?

LLQ pain, bloody diarrhea

A

ulcerative colitis

329
Q

Crohn’s disease or ulcerative colitis?

crypt abscesses with neutrophils, ulcers, bleeding, no granulomas (Th2 mediated)

A

ulcerative colitis

330
Q

Crohn’s disease or ulcerative colitis?

noncaseating granulomas and lymphoid aggregates (Th1 mediated)

A

Crohn’s disease

331
Q

Crohn’s disease or ulcerative colitis?

skip lesions

A

Crohn’s disease

332
Q

Crohn’s disease or ulcerative colitis?

continuous colonic lesions, always with rectal involvement

A

ulcerative colitis

333
Q

Crohn’s disease or ulcerative colitis?

rectal sparing

A

Crohn’s disease

334
Q

Crohn’s disease or ulcerative colitis?

pyoderma gangrenosum, primary sclerosing cholangitis, ankylosing spondylitis, uveitis, p-ANCA positive

A

ulcerative colitis

335
Q

Crohn’s disease or ulcerative colitis?

RLQ pain, nonbloody diarrhea

A

Crohn’s disease

336
Q

Crohn’s disease or ulcerative colitis?

complications of strictures, fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer

A

Crohn’s disease

337
Q

Crohn’s disease or ulcerative colitis?
complications of malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (worse with right-sided colitis or pancolitis, seen at >10 years of disease)

A

ulcerative colitis

338
Q

Crohn’s disease or ulcerative colitis?

migratory polyarthritis, erythema nodosum, ankylosing sponylitis, uveitis, kidney stones

A

Crohn’s disease

339
Q

Crohn’s disease or ulcerative colitis?

older patients

A

ulcerative colitis

340
Q

Crohn’s disease or ulcerative colitis?

autoimmune pathogenesis

A

ulcerative colitis

341
Q

Crohn’s disease or ulcerative colitis?

superificial mucosal and submucosal inflammation only; friable mucosal psuedopolyps with freely hanging mesentery

A

ulcerative colitis

342
Q

Crohn’s disease or ulcerative colitis?

loss of haustra leads to a “lead pipe” appearance on imaging

A

ulcerative colitis

343
Q

Crohn’s disease or ulcerative colitis?

transmural inflammation; cobblestone mucosa, creeping fat, bowel wall thickening

A

Crohn’s disease

344
Q

Crohn’s disease or ulcerative colitis?

“string sign” on barium swallow X-ray, linear ulcers, fissures, perianal fistulas, abscesses

A

Crohn’s disease

345
Q

What are the possible treatments for Crohn’s disease?

A 
corticosteroids
azathioprine
MTX
infliximab
adalimumab
346
Q

What are the possible treatments for ulcerative colitis?

A

ASA preparations (sulfasalazine, mesalamine)
6-mercaptopurine
infliximab
colectomy

347
Q

Smoking is a protective action against what disease?

A

ulcerative colitis

348
Q

What are the requirements for a diagnosis of irritable bowel syndrome?

A 
6 months of the following:
recurrent abdominal pain, occurring at least 3 days per month, with two or more of the following:
-pain improves with defecation
-change in stool frequency
-change in appearance of stool

May present with diarrhea, constipation, or alternating symptoms.

349
Q

What can trigger an episode of irritable bowel syndrome?

A

caffeinated beverages
high fat foods
raw fruits and vegetables

350
Q

Among which group is irritable bowel syndrome more common?

A

middle-aged women

351
Q

What causes acute appendicits in adults?

A

obstruction due to fecalith

352
Q

What causes acute appendicitis in children?

A

obstruction due to lymphoid hyperplasia

353
Q

What are the clinical features of acute appendicitis?

A

periumbilical pain, eventually localizing to RLQ at McBurney point
fever
nausea
RUPTURE –> guarding and rebound tenderness

354
Q

What is the common complication of acute appendicitis?

A

periappendiceal abscess

355
Q

Where is McBurney’s point?

A

1/3 the distance from the ASIS to umbilicus

356
Q

What is the differential diagnosis for acute appendicitis?

A

elderly patient: diverticulitis

female patient: ectopic pregnancy (beta-HCG to rule out)

357
Q

What is a diverticulum, where is it most common, and how do you differentiate “true” from “false”?

A

DEFINITION blind pouch protruding from the alimentary tract that communicates with the lumen of the gut
LOCATION sigmoid colon, where vasa recta perforate the muscularis externa
TRUE all three gut wall layers outpouch
FALSE aka pseudodiverticulum; only mucosa and submucosa outpouch

358
Q

Which are more common, true or flase diverticula?

A

false, seen in the esophagus, stomach, duodenum, and colon; they lack (or have an attenuated) muscularis externa

359
Q

What are the risk factors for colonic diverticula?

A

constipation
straining
low-fiber diet
increased age

360
Q

What is the pathogenesis of diverticulosis? What are its complications?

A

PATHOGENESIS increased intralumincal pressure, focal weakness in the colonic wall –> many false diverticula
COMPLICATIONS diverticulitis, fistulas

361
Q

What is the presentation of diverticulosis?

A

often asymptomatic
vague discomfort
hematochezia

362
Q

In which population is diverticulosis common?

A

> 60 (seen in 50%)

363
Q

What are the symptoms of diverticulitis?

A

LLQ pain (“left-sided appendicitis”)
fever
leukocytosis
stool occult blood, with or without hematochezia

364
Q

What are the complications of diverticulitis?

A

PERFORATION –> peritonitis, abscess formation, bowel stenosis
COLOVESICAL FISTULA –> pneumaturia

365
Q

As it presents similarly to another disease, what is diverticulitis commonly caused?

A

“left-sided appendicitis”

366
Q

What is normally seen upon stool sample of diverticulitis?

A

occult blood is common, with or without hematochezia

367
Q

Where does a herniation of Zenker’s diverticulum occur?

A

Killian’s triangle between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor

368
Q

What is the embyrologic origin of Meckel’s diverticulum?

A

persistence of the vitelline duct (failure to involute)

369
Q

What type of diverticulum is Meckel’s, and what may it contain?

A

true (all three layers of bowel); may contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue

370
Q

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

A

Meckel’s diverticulum

371
Q

What is the presentation of Meckel’s diverticulum?

A 
most cases are asymptomatic 
melena 
RLQ pain 
intussusception 
volvulus 
obstruction near the terminal ileum 
bleeding due to heterotropic gastric mucosa
372
Q

What is an omphalomesenteric cyst?

A

cystic dilation of the vitelline duct

373
Q

How is Meckel’s diverticulum diagnosed?

A

pertechnetate study for ectopic uptake

374
Q

What are the “5 2’s” of Meckel’s diverticulum?

A 
2 inches long 
2 feet from the ileocecal valve 
2% of the population 
2 years of life 
2 types of epithelia (gastric and pancreatic)
375
Q

What is the pathogenesis of intussusception?

A

telescoping of one bowel segment into a distal segment (commonly at the ileocecal junction) –> peristalsis pulls segment forward –> obstruction –> “currant jelly” stools, compromised blood supply with infarction

376
Q

In an adult, with what is intussusception associated?

NOTE the majority of cases are in children

A

intraluminal mass or tumor

377
Q

In a child, with what is intussusception associated?

A

usually idiopathic; rotavirus or adenovirus –> lymphoid hyperplasia of the terminal ileum –> intussusception into the cecum

378
Q

What is the pathogenesis of a volvulus, where is it more common, and in what population is it more common?

A

PATHOGENESIS twisting of bowel along its mesentery –> obstruction, infarction
LOCATION sigmoid colon and cecum, where there is redundant mesentery EPIDEMIOLOGY usually in the elderly

379
Q

In what population of patients is Hirschsprung’s disease common?

A

Down syndrome

380
Q

What is the pathogenesis of Hirschsprung’s disease?

A

failure of neural crest cell migration –> lack of ganglion cells / enteric nervous plexuses (Auerbach’s, Meissner’s) –> defective relaxation and peristalsis of rectum and distal sigmoid colon –> congenital megacolon (dilated portion of colon proximal to aganglionic segment, “transition zone”)

381
Q

What is the presentation of Hirschsprung’s disease?

A 
failure to pass meconium
chronic constipation early in life
empty rectal vault on digital rectal exam
massive dilation (megacolon) of bowel proximal to obstruction with risk for rupture
382
Q

What is the treatment of Hirschprung’s disease?

A

resection of the involved bowel

383
Q

With what is duodenal atresia associated?

A

Down syndrome

384
Q

What is the pathogenesis of duodenal atresia?

A

failure of recanalization of small bowel –> early bilious vomiting with proximal stomach distention (“double-bubble” on X-ray

385
Q

What is meconium ileus, and with what is it associated?

A

DEFINITION meconium plug obstructs intestine –> no stool passage at birth
ASSOCIATION cystic fibrosis

386
Q

What is necrotizing enterocolitis, and with what is it associated?

A 
DEFINITION necrosis of intestinal mucosa and possible perforation; usually involving colon, but may involve entire GI tract 
ASSOCIATION prematurity (decreased immunity)
387
Q

Where does ischemic colitis normally occur?

A 
splenic flexure (watershed area of the SMA)
distal colon
388
Q

What population is typically affected by ischemic colitis?

A

the elderly

389
Q

What is the common pathogenesis of ischemic bowel disease?

A

atherosclerosis of SMA –> ischemic damage to splenic flexure at watershed area –> infarction

390
Q

What is the presentation of ischemic colitis / ischemic bowel disease?

A

sudden abdominal pain, normally in the background of cardiovascular disease
bloody diarrhea
nausea, vomiting
pain after eating –> weight loss

391
Q

What is the most common cause of small bowel obstruction?

A

adhesion

392
Q

What is the pathogenesis of adhesions?

A

surgery –> fibrous band of scar tissue –> well-demarcated necrotic zones –> small bowel obstruction

393
Q

Where does angiodysplasia commonly arise and why?

A

LOCATION cecum, terminal ileum, ascending colon

REASON high wall tension

394
Q

What is the pathogenesis fo angiodysplasia?

A

acquired malformation of mucosal and submucosal capillary beds –> tortuous dilation of vessels –> rupture–> hematochezia

395
Q

How common is angiodysplasia overall, and in which populations is it common?

A

OVERALL <1% of cases

AFFECTED POPULATION older patients; 20% of patients with lower abdominal bleed

396
Q

What is the inheritance pattern of hereditary hemorrhagic telangiectasia?

A

autosomal dominant

397
Q

What is the pathogenesis of hereditary hemorrhagic telangiactasia?

A

thin-walled blood vessels –> rupture –> bleeding in mouth, GI tract

398
Q

What is a colonic polyp? Are they commonly malignant or benign, and what is their appearance?

A

DEFINITION raised protrusions of colonic mucosa into gut lumen –> sawtooth appearance
BENIGN 90% are non-neoplastic
APPEARANCE rectosigmoid; tubular or villous

–VILLOUS is most likely VILLainOUS–

399
Q

What is the most common type of polyp, and how does this type of polyp appear histologically?

A

hyperplastic

HISTOLOGY rectosigmoid; hyperplasia of glands; “serrated” appearance on microscopy

400
Q

What is the second most common type of polyp?

A

adenomatous

401
Q

Which type of colon polyp is malignant? What increases the risk of malignancy?

A

adenomatous

RISK >2 cm in size size, villous histology, increased epithelial dysplasia with sessile (flat) growth

402
Q

What are the symptoms of polyps?

A 
often asymptomatic
lower GI bleed
partial obstruction
secretory diarrhea
positive test for fecal occult blood
remove all polyps seen on colonoscopy
403
Q

What molecular mutations are involved in the adenoma-carcinoma sequence?

A

APC (sporadic or germline): decreased intercellular adhesion, increased proliferation –> increased risk for polyp formation
K-ras: unregulated intracellular signal transduction –> formation of polyp
p53: increased tumorigenesis –> progression to carcinoma
increased COX expression: progression to carcinoma

–AK-53–

404
Q

What pharmaceutical can impede progression from adenoma to carcinoma?

A

aspirin (impedes COX)

405
Q

In what population are juvenile polyps seen? In which portion of the GI tract are they found?

A 
EPIDEMIOLOGY <5 years
LOCATION rectum (80%)
406
Q

What is juvenile polyposis syndrome?

A

multiple juvenile polyps in STOMACH and colon

confers increased risk for progression to carcinoma

407
Q

What is the inheritance of Peutz-Jeghers syndrome?

A

autosomal dominant

408
Q

What is the appearance of Peutz-Jeghers? With what is it associated?

A

APPEARANCE hamartomatous polyps throughout GI tract; hyperpigmented (freckle-like) mouth, lips, hands, genitalia skin
ASSOCIATIONS increased risk for colorectal, breast, and gynecologic cancer

409
Q

What is the inheritance pattern of FAP (familial adenomatous polyposis)?

A

autosomal dominant, APC mutation on chromosome 5

2-hit hypothesis

410
Q

What is the pathogenesis and treatment of FAP?

A

PATHOGENESIS mutation of APC on chromosome 5q –> hundreds to thousands of adenomatous colonic polyps, ALWAYS involving the rectum –> 100% progress to colorectal cancer
TREATMENT prophylactic removal of colon and rectum

411
Q

What is Gardner syndrome?

A

FAP with fibromatosis and osteomas
FIBROMATOSIS non-neoplastic proliferation of fibroblasts, arises in retroeritoneum (desmoid) and locally destroys tissue; congenital hypertrophy of retinal pigment epithelium
OSTEOMA benign tumor of bone, arising in the skull

412
Q

What is Turcot syndrome?

A

FAP with CNS tumors (medulloblastoma and glial tumors)

–TUrcot = TUrban–

413
Q

What is the third most common cancer in the US?

A

colorectal cancer

414
Q

What is the third deadliest cancer in the US?

A

colorectal cancer

415
Q

What is the epidemiology of colorectal cancer?

A

> 50 (peak incidence 60-70)

~25% have a family history

416
Q

What are the four genetic associations with colorectal cancer?

A

FAP
Garner’s syndrome
Turcot’s syndrome
HPNCC (hereditary nonpolyposis colorectal cancer)/Lynch syndrome

417
Q

What is the inheritance pattern of HPNCC?

A

autosomal dominant

418
Q

What is the mutation in HPNCC?

A

DNA mismatch repair genes

419
Q

Most colorectal cancers show what mutation (85%)?

A

APC/Beta-catenin/WNT signaling pathway

may be combined with DNA mismatch repair mutations

420
Q

What area of the GI tract is ALWAYS involved in HPNCC? How often does HPNCC progress to colorectal cancer?

A

LOCATION proximal colon is ALWAYS involved

PROGRESSION 80% of cases; please note that this progression is NOT linked to adenomaous polyps, but arises de novo

421
Q

What is the most common pathogenesis for colorectal cancer (85%)?

A

adenoma-carcinoma sequence via APC/beta-catenin/WNT pathway

422
Q

What is the second common pathogenesis for colorectal cancer (15%)?

A

microsatellite instability
repeating sequences of noncoding DNA –> mutation in DNA mismatch repair enzymes –> instability of DNA sequence (integrity is not maintained) –> HPNCC –> increased risk for colorectal, ovarian, and endometrial cancers

423
Q

When should screening for colorectal cancer begin for American patients?

A

50 by colonoscopy and fecal occult blood testing

424
Q

How does colorectal cancer arising from a colitis-associated state differ from sporadic cases?

UWORLD OBJECTIVE

A

younger patients
progression from flat and non-polypoid dysplasia
histologically: mucinous and/or signet ring
early p53, late APC gene mutations
distribution in proximal colon
multifocal in nature

425
Q

What is the presentation of left-sided (descending) colorectal carcinoma?

A 
"napkin-ring" lesion, infiltrating mass
decreased stool caliber
partial obstruction
LLQ pain, colicky
blood-streaked stool
426
Q

What is the presentation of right-sided (ascending) colorectal carcinoma?

A

raised lesion, exophytic mass
iron-deficiency anemia (occult bleeding)
vague pain
weight loss

427
Q

What is the first suspicion if an older adult presents with iron deficiency anemia, whether male or postmenopausal female?

A

colorectal cancer UNTIL proven otherwise

428
Q

Colonic carcinoma confers an additional risk for what type of bacterial infection?

A

S. bovis endocarditis

429
Q

What are the major risk factors, aside from genetics, for colorectal cancer?

A 
IBD
tobacco use
large villous adenomas
juvenile polyposis syndrome
Peutz-Jeghers syndrome
430
Q

What tumor markers is useful for assessing treatment response and detecting recurrence?

NOTE this marker is NOT useful for screening!

A

CEA

431
Q

What is seen upon barium enema X-ray in colorectal cancer?

A

apple-core lesion

432
Q

What is a carcinoid tumor?

A

malignant proliferation of neuroendocrine cells of low-grade malignancy –> submucosal polyps-like nodule –> secretion of 5-HT –> serotonin released into portal circulation –> liver monoamine oxidase metabolizes serotonin to 5-HIAA –> excreted in urine

433
Q

Where are carcinoid tumors commonly seen?

A

appendix
ileum (most common)
rectum

434
Q

What are the conditions for carcinoid tumor to progress to carcinoid syndrome? What is the process?

A

metastasis of carcinoid tumor –> serotonin bypasses liver metabolism –> serotonin released into heatic vein –> hepato-systemic shunt leaks serotonin into systemic circulation –> carcinoid syndrome and heart disease

435
Q

What is the presentation of carcinoid syndrome (not including heart disease)?

A

bronchospasm with wheezing
diarrhea
flushing of skin

NOTE this can be triggered by alcohol or emotional stress, leading to serotonin release by the tumor

436
Q

What is the presentation of carcinoid heart disease?

A

increased collagen –> right-sided valvular fibrosis –> tricuspid regurgitation, pulmonary valve stenosis

437
Q

Why are left-sided lesions not seen in carcinoid heart disease?

A

monoamine oxidase is also released by the lung, allowing the serotonin to be metabolized

438
Q

How are the lab findings in carcinoid syndrome?

A

elevated plasma serotonin levels

urinary 5-hydroxyendoleactic acid

439
Q

What is the presentation of portal HTN?

A 
esophageal varices --> hematemesis
peptic ulcer
(both of the above cause) melena
congestive splenomegaly/hypersplenism
caput medusae 
ascites
portal hypertensive gastropathy
hemorrhoids
hepatic encephalopathy
440
Q

What is the presentation of liver cell failure (cirrhosis)?

A 
coma
scleral icterus
fetor hepaticus (breath smells musty)
spider nevi
gynecomastia (irreversible)
jaundice
palmar erythema
testicular atrophy
liver "flap" causing asterixis (coarse hand tremor)
bleeding tendency (decreased clotting factors, increased PTT)
anemia
hypoalbuminemia --> ankle edema
441
Q

What is the histological appearance of cirrhosis?

A

diffuse fibrosis
nodular regeneration
destruction of normal architecture of liver

442
Q

How is fibrosis mediated in cirrhosis?

A

stellate cells (beneath endothelial cells lining sinusoids) release TGF beta

443
Q

What are the causes of cirrhosis?

A

alcohol (60-70%)
viral hepatitis
biliary disease
hemochromatosis

444
Q

How do liver enzymes respond to alcoholic hepatitis?

A

AST > ALT (ratio > 1.1)

445
Q

How do liver enzymes respond to viral hepatitis?

A

ALT > AST

446
Q

For what issues is alkaline phosphatase (ALP) useful?

A

obstructive liver disease (hepatocellular carcinoma)
bone disease
bile duct disease

447
Q

In which issues does GGT (gamma-gluatmyl transpeptidase) increase?

A

various liver and biliary diseases, NOT bone disease

448
Q

For which issues is amylase useful?

A

acute pancreatitis

mumps

449
Q

For which issues is lipase useful?

A

acute pancreatitis

450
Q

In which issue does ceruloplasmin decrease?

A

Wilson’s disease

451
Q

What are the findings in Reye’s syndrome?

A 
mitochondrial abnormalities
fatty liver (microvesicular fatty changes)
hypoglycemia
vomiting
hepatomegaly
coma
452
Q

With what is Reye’s syndrome associated?

A

viral infection (VSV, influenza B) treated with aspirin

453
Q

What is the mechanism of aspirin in Reye’s syndrome?

A

reversible inhibition of mitochondrial enzyme –> decreased beta-oxidation

454
Q

How many alcoholics develop alcoholic cirrhosis?

A

10-20%

455
Q

What is the histologic appearance of hepatic steatosis?

A

macrovesicular fatty change, periventricular with progression to all zones
intracytoplasmic vacuoles
giant mitochonria
no necrosis, no inflammation

456
Q

What causes hepatic steatosis?

A

moderate alcohol intake; may be reversible with cessation

457
Q

What causes alcoholic hepatitis?

A

sustained, long-term consumption of alcohol

458
Q

What is the histologic appearance of alcoholic hepatitis?

A

ballooning degeneration
sclerosing hyaline necrosis
neutrophilic infiltration
Mallory bodies (intracytoplasmic eosinophilic inclusions)

459
Q

What is the presentation of alcoholic hepatitis?

A 
malaise
anorexia
weight loss
tender hepatomegaly
cholestasis
fulminant liver failure
460
Q

What is the histologic appearance of alcoholic cirrhosis?

A

micronodular, irregularly shrunken liver
“hobnail” appearance
sclerosis around central vein (Zone III)

NOTE damage is mediated by acetaldehyde

461
Q

What is NAFLD?

A

non-alcoholic fatty liver disease
fatty change, hepatitis, and/or cirrhosis without exposure to alcohol or other known insult

1st hit leads to steatosis; increased insulin resistance, increased fatty acids
2nd hit leads to NASH with lipid peroxidation

462
Q

What is the association of NAFLD?

A

obesity

463
Q

What is the presentation of NAFLD? How is it diagnosed?

A

PRESENTATION largely asymptomatic, hepatosplenomegaly, fatigue, RUQ pain, edema, pruritis, GI bleed, ascites
DIAGNOSIS of exclusion; ALT > AST (note that this is opposite that of alcoholic cirrhosis)

464
Q

What is the most common primary malignant tumor of the liver in adults?

A

hepatocellular carinoma/hepatoma

465
Q

With what is hepatocellular carcinoma associated?

A

hepatitis B worldwide, hepatitis C in the West
Wilson’s disease
hemochromatosis
alpha-1 antitrypsin deficiency
alcoholic cirrhosis
carcinogens (Aspergillus aflatoxin induces p53 mutations)

466
Q

What is the presentation of hepatocellular carcinoma?

A 
jaundice
tender hepatomegaly
ascites
polycythemia
hypoglycemia
pale or green appearing liver (due to bile prodution)
increased alpha-fetoprotein (AFP)
vascular invasion --> hematogenous dissemination --> hepatic vein --> right heart involvement, Budd-Chiari syndrome,
467
Q

What are the factors of the fibrolamellar variant of hepatocellular carcinoma?

A

EPIDEMIOLOGY 20-40 years
ASSOCIATIONS none
HISTOLOGY cords of well-defined hepatocytes; parallel bands of fibrosis

468
Q

With what fungi is hepatocellular carcinoma associated?

A

Aspergillus (produces aflatoxin, which induces p53 mutations)

469
Q

What is a cavernous hemangioma?

A

DEFINITION common, benign liver tumor
EPIDEMIOLOGY 30-50 years

NOTE do NOT biopsy (risk of hemorrhage)

470
Q

What is a hepatic adenoma? How does it appear histologically, and what risks does it carry?

A

DEFINITION benign liver tumor
ASSOCIATIONS oral contraceptive or steroid use
HISTOLOGY circumscribed, not encapsulated; no portal tracts in lesion
COMPLICATIONS risk of rupture and intraperitoneal bleeding, especially during pregnancy

471
Q

What is an angiosarcoma?

A

EPIDEMIOLOGY 60-70 years, males > females DEFINITION malignant tumor of endothelial origin, malignant in under 7 years
ASSOCIATIONS exposure to arsenic or polyvinyl chloride
HISTOLOGY involves entire liver

472
Q

How does nutmeg liver appear histologically, and what causes it? To what may it progress?

A

HISTOLOGY backup of blood into liver –> mottled appearance
CAUSES right-sided heart failure, Budd-Chiari syndrome
COMPLICATIONS centrilobular congestions, necrosis –> cardiac cirrhosis

473
Q

Why is centrilobular necrosis of the liver more common than that of other zones?

A

Zone III is the most hypoxic zone

474
Q

What is the pathogenesis of Budd-Chiari syndrome?

A

occlusion of IVC or hepatic veins –> centrilobular congestion, necrosis –> congestive liver failure –> infarction

475
Q

What is the presentation of Budd-Chiari syndrome?

A 
hepatomegaly
ascites
RUQ pain
abdominal pain
eventual liver failure
possible, varices
NO JVD
476
Q

With what is Budd-Chiari syndrome associated?

A 
hypercoagulable state
polycythemia vera
pregnancy
hepatocellular carcinoma
oral contraceptive use
paroxysmal nocturnal hemoglobinuria
477
Q

How is Budd-Chiari syndrome usually diagnosed? What is the gold standard for diagnosis?

A

USUALLY ultrasound doppler

GOLD STANDARD angiography (expensive)

478
Q

Does portal vein thrombosis present with or without ascites?

A

WITHOUT

479
Q

What is the pathogenesis of alpha-1 antitrypsin deficiency?

A

autosomal recessive inheritance of PiZZ gene –> misfolded gene product –>
in liver: protein aggregates in hepatocellular ER –> cirrhosis with PAS-positive, diastase-resistant globules in liver
in lungs: lack of functioning enzyme –> decreased elastic tissue –> panacinar emphysema

480
Q

What causes jaundice?

A

elevated bilirubin (>2 mg/dL) –> yellow skin and/or sclerae, as caused by the following:

  1. direct hepatocellular injury
  2. obstruction to bile flow
  3. hemolysis
481
Q

If the jaundice is hepatocellular, what is the type of hyperbilirubinemia, urine bilirubin, and urine urobilinogen?

A

HYPERBILIRUBENEMIA direct or indirect (conjugated or unconjugated)
URINE BILIRUBIN increased
URINE UROBILINOGEN normal or decreased

482
Q

If the jaundice is hepatocellular, what is the type of hyperbilirubinemia, urine bilirubin, and urine urobilinogen?

A

HYPERBILIRUBENEMIA direct (conjugated)
URINE BILIRUBIN increased
URINE UROBILINOGEN decreased

483
Q

If the jaundice is hepatocellular, what is the type of hyperbilirubinemia, urine bilirubin, and urine urobilinogen?

A

HYPERBILIRUBENEMIA indirect (unconjugated)
URINE BILIRUBIN absent (acholuria)
URINE UROBILINOGEN increased

484
Q

What is the process of normal bilirubin metabolism?

A

RBCs consumed by macrophages of the reticuloendothelial system –> protoporphyrin from heme is converted to unconjugated bilirubin –> unconjugated bilirubin is carried by albumin to liver –> uridine glucuronyl transferase in hepatocytes conjugates bilirubin –> conjugated bilirubin is transferred to bile canaliculi to form bile –> bile is stored in gallbladder –> gallbladder releases bile into small bowel to aid in digestion –> intestinal flora convert conjugated bilirubin to urobilinogen –> urobilinogen is either excreted in stool (thus brown) or partially reaborbed into blood and filtered by kidney –> kidney oxidizes urobilinogen to urobilin –> urobilin is excreted in urine (thus yellow)

485
Q

Which is water soluble: conjugated or unconjugated bilirubin?

A

conjugated biliruin; excreted in urine and, thus, less toxic

486
Q

Which is water insoluble: conjugated or unconjugated bilirubin?

A

unconjugated; may diffuse into tissues

NOTE this causes kernicterus in neonates and is, thus, of specific concern

487
Q

What is the differential diagnosis for unconjugated hyperbilirubinemia?

A

hemolytic anemia, hemoglobinopathies, systemic infections

Gilbert’s syndrome, neonatal jaundice

488
Q

What is the differential diagnosis for conjugated hyperbilirubinemia?

A

viral, drug, alcohol injury to liver
cirrhosis, gall stones, carcinoma, pancreatitis
Dubin-Johnson syndrome

489
Q

Name the cause, laboratory findings, and clinical features of extravascular hemolysis or ineffective erythropoiesis?

A

CAUSE high levels of unconjugated bilirubin overwhelm the conjugating ability of the lvier
LABS increased unconjugated bilirubin

490
Q

Name the cause, laboratory findings, and clinical features of physiologic jaundice of the newborn? How is it treated?

A

CAUSE transiently low UDP-glucuronyl transferase
LABS increased unconjugated bilitrubin
PRESENTATION jaundice; kernicterus (fat soluble –> crosses incomplete BBB –> deposition in basal ganglia –> irreversible neurological deficits, possible death; may be exacerbated by breast feeding (glucuronidates, low vitamin K)
TREATMENT phototherapy, which converts unconjugated bilirubin to its water-soluble form, causing deposition in the skin

491
Q

Name the cause, laboratory findings, and clinical features of Gilbert syndrome.

A

CAUSE research is not conclusive as to inheritance pattern, but genetic reduction in activity of UDP-glucuronyl transferase
LABS increased unconjugated bilirubin without overt hemolysis; bilirubin increases with fasting and stress
PRESENTATION no clinical consequences beyond stress-induced jaundice

492
Q

Name the cause, laboratory findings, and clinical features of Crigler-Najjar syndrome. What is its treatment?

A

CAUSE absence of UDP-glucuronyl transferase; Type I more severe than Type II
LABS increased unconjugated bilirubin
PRESENTATION early life; jaundice, kernicterus, fatal within a few years in Type I
TREATMENT plasmapheresis, phototherapy; Type II responds to phenobarbital (increases liver enzyme synthesis)

493
Q

Name the cause, laboratory findings, and clinical features of Dubin-Johnson syndrome.

A

CAUSE autosomal recessive deficiency of bilirubin canalicular transport protein –> defective liver excretion
LABS increased conjugated bilirubin, normal liver enzyme tests
PRESENTATION asymptomatic, grossly black liver, not clinically significant

494
Q

Name the cause, laboratory findings, and clinical features of Rotor syndrome.

A

CAUSE autosomal recessive decrease of bilirubin canalicular transport protein –> low liver excretion
LABS increased conjugated bilirbuin, normal liver enzyme tests
PRESENTATION asymptomatic and even milder than Dubin-Johnson syndrome; no black liver; not clinically significant

495
Q

Name the cause, laboratory findings, and clinical features of biliary tract obstruction (obstructive jaundice).

A

ASSOCIATIONS/CAUSE gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, liver fluke (Clonorchis sinesis)
LABS increased conjugated bilirubin, decreased urine urobilinogen, increased alkaline phosphatase
PRESENTATION dark urine (bilirubinuriia), pale stool, pruritis (increased plasma bile acids), hypercholesterolemia with xanthomas, steatorrhea with malabsorption of fat-soluble vitamins

496
Q

Name the cause, laboratory findings, and clinical features of viral hepatitis.

A

CAUSE viral inflammation –> disruption of hepatocytes and small bile ductules
LABS increased conjugated and unconjugated bilirubin, elevated AST and ALT (ratio <1.1)
PRESENTATION dark urine (bilirubinuria), fever, jaundice

497
Q

Name the single-stranded hepatitis virus strain(s).

A

HAV
HCV
HDV
HEV

498
Q

Name the double stranded hepatitis virus strain(s).

A

HBV
This virus has its own DNA-dependent DNA polymerase to make full dsDNA. Host RNA polymerase transcribes mRNA from viral DNA, then makes viral proteins from the mRNAs.

499
Q

Which hepatitis virus strains are transmitted fecally-orally?

A

HAV, commonly acquired by travelers

HEV, commonly acquired from contaminated water or undercooked seafood

500
Q

Which hepatitis virus strains are transmitted parenterally?

A

HBV

HDV

501
Q

Which hepatitis virus strains are transmitted sexually?

A

HBV

HDV

502
Q

What is the transmission pattern for HCV?

A

primarily blood: IV drug use, post-transfusion

503
Q

Which hepatitis virus strains are transmitted maternally?

A

HBV

HDV

504
Q

Which hepatitis virus strain is most likely to become epidemic?

A

HEV

-Enteric, Endemic regions, Epidemic, Expectant mothers–

505
Q

Which hepatitis virus strains do not have an envelope? How does this affect their infectivity?

A

HAV, HEV
no gut destruction

–the VOWELS affect your BOWELS–

506
Q

Which hepatitis virus strains carry a risk for hepatocellular carcinoma?

A

HBV, which integrates into the host chromosome, acting as an oncogene
HCV, leading to chronic inflammation
HDV

507
Q

Which has a poorer prognosis: coinfection of HDV and HBV, or HBV superinfection with HDV?

A

superinfection

508
Q

What does anti-HAV IgM indicate?

A

active hepatitis A

509
Q

What does anti-HAV IgG indicate?

A

prior HAV infection and/or vaccination

patient protected against reinfection

510
Q

What does HBsAg, when found alone, indicate?

A

hepatits B infection, virus is present but not infective

511
Q

What does anti-HBs indicate?

A

immunity to hepatitis B, by vaccination or otherwise

512
Q

What does HBcAg indicate?

A

core HBV present

513
Q

What does anti-HBc IgM indicate?

A

acute/recent infection with HBV

514
Q

What does anti-HBc IgG indicate?

A

prior exposure or chronic HBV infection

515
Q

What does HBeAg indicate?

A

active HBV viral repetition with high transmissibility

516
Q

What does anti-HBe indicate?

A

low transmissibility of HBV

517
Q

From acute to recovery, as well as immunized, what serologic markers are present in HBV infection?

A

ACUTE HBsAg, HBeAg (infectivity), anti-HBc IgM
WINDOW anti-HBe, anti-HBc IgM
CHRONIC, HIGH INFECTIVITY HBsAg, HBeAg (infectivity), anti-HBc IgG
CHRONIC, LOW INFECTIVITY HBsAg, anti-HBe, anti-HBc IgG
RECOVERY anti-HBs, anti-HBe, anti-HBc IgG
IMMUNIZED anti-HBs
–order of appearance: antigensSEantibodiesCES–

518
Q

How does the liver appear in hepatitis?

A

inflammation involving liver lobules and portal tracts
apoptosis of hepatocytes
if caused by HBV: “ground glass”
if caused by HCV: steatosis

519
Q

Besides hepatitis virus strains, what can cause viral hepatitis?

A

EBV

CMV

520
Q

Which pharmaceuticals are hepatotoxic?

A

acetaminophen: centrilobular to massive hepatocyte necrosis
carbon tetrachloride from Amanita mushroom toxin: centrilobular to massive hepatocyte necrosis
tetracycline: microvesicular steatosis

521
Q

What molecular mutation is involved in Wilson’s disease?

A

autosomal recessive defect in the ATP7B gene on chromosome 13 for ATP-mediated hepatocyte copper transport

522
Q

What is the pathogenesis of Wilson’s disease?

A

autosomal recessive defect in ATP7B –> lack of copper transport into bile, lack of copper incorporation into ceruloplasmin –> copper buildup in hepatocytes –> copper leak into serum –> copper deposition in tissues (liver, brain, kidneys, joints) –> copper-mediated production of hydroxyl free radicals –> tissue damage

523
Q

What is the presentation of Wilson’s disease?

A 
Cirrhosis
decreased serum Ceruloplasmin
Corneal deposition (Kayser-Fleisher rings)
Copper accumulation (increased urinary copper, copper seen on liver biopsy)
Carcinoma, hepatocellular
Hemolytic anemia
Basal ganglia degeneration (behavioral changes, Parkinsonian symptoms)
Asterixis
Dementia
Dyskinesia
Dysarthria
--CCCCCopper is Hella BADDD---
524
Q

How does the liver appear in Wilson’s disease?

A

deposition of copper

macronodular sclerosis

525
Q

What is the treatment of Wilson’s disease?

A

D-penicillamine, a copper chelator

526
Q

What results from a mutation in ATP7B? And in ATP7A?

A

7B Wilson’s disease, autosomal recessive
7A Menkes kinky hair disease, X-linked recessive (this is an abnormal intestinal copper absorption issue appearing in infancy)

527
Q

What is the normal total body iron level? What level is seen in hemochromatosis?

A

NORMAL .5 g

HEMOCHROMATOSIS may reach 50g (sets of metal detectors)

528
Q

What is the pathogenesis of hemochromatosis?

A

chronic transfusions (B thalassemia major) or autosomal recessive defect in iron absorption –> excess body iron –> hemosiderosis (deposition in tissues) –> generation of free radicals –> hemochromatosis (organ damage)

529
Q

What is the genetic basis for primary hemochromatosis?

A

mutations in the HFE gene, usually C282Y or H63D (cysteine replaced by tyrosine at 282)
also associated with HLA-A3

530
Q

What is the presentation of hemochromatosis?

A

EPIDEMIOLOGY 5th-6th decade
SYMPTOMS triad: micronodular cirrhosis, secondary DM, bronze skin; additionally, CHF, cardiomyopathy, cardiac arrhythmias; testicular atrophy –> gonadal dysfunction; psuedogout, arthritis
LABS increased ferritin, decreased TIBC, increased serum iron, increased % saturation
liver biopsy shows accumulation of brown pigment tin hepatocytes; Prussian blue distinguishes iron (blue) from lipofuscin

531
Q

What is the major complication of hemochromatosis?

A

hepatocellular carinoma

532
Q

What is the treatment of hemochromatosis?

A

repeated phlebotomy
deferasirox
deferoxamine

533
Q

How much liver must be functionally lost for hepatic failure to become symptomatic?

A

80-90%

534
Q

Name the presentation for secondary biliary cirrhosis, primary biliary cirrhosis, and primary sclerosing cholangitis.

A 
pruritus
jaundice
dark urine
light stools
hepatosplenomegaly
535
Q

Name the labs for secondary biliary cirrhosis, primary biliary cirrhosis, and primary sclerosing cholangitis.

A

increased conjugated bilirubin
increased cholesterol
increased alkaline phosphatase

Primary biliary cirrhosis demonstrates hypocomplementemia and immune complexes
Primary sclerosing cholangitis demonstrates p-ANCA

536
Q

What is the pathophysiology of secondary biliary cirrhosis?

A

gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreatic head
–> extrahepatic biliary obstruction –> increased pressure in intrahepatic ducts –> injury/fibrosis and bile stasis

537
Q

What is the epidemiology and pathophysiology of primary biliary cirrhosis?

A

EPIDEMIOLOGY women 6:1, 40 years

PATHOPHYSIOLOGY autoimmune destruction of INTRAHEPATIC bile ducts –> lymphocytic infiltrate with granulomas

538
Q

What is the epidemiology and pathophysiology of primary sclerosing cholangitis?

A

EPIDEMIOLOGY men 2:1, 3rd-5th decade
PATHOPHYSIOLOGY unknown cause of concentric “onion skin” bile duct fibrosis –> segmental strictures and dilation with “beading” of INTRA- AND EXTRAHEPATIC bile ducts on ERCP

539
Q

By what may secondary biliary cirrhosis be complicated?

A

ascending cholangitis

540
Q

What labs are specific to primary biliary cirrhosis? With what is primary biliary cirrhosis associated?

A

LABS increased serum mitochondrial antibodies, including IgM

ASSOCIATIONS celiac disease, RA, CREST

541
Q

What labs are specific to primary sclerosing cholangitis? With what is it associated? Finally, does primary sclerosing cholangitis confer an increased risk for any other issue?

A

LABS hypergammaglobulinemia (IgM)
ASSOCIATIONS ulcerative colitis, secondary biliary cirrhosis
INCREASED RISK cholangiocarcinoma

542
Q

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

A

colon
pancreas
lung
breast

543
Q

What is biliary atresia, and how does it present?

A

DEFINITION failure to form (or early destruction of) extrahepatic biliary tree
PRESENTATION biliary obstruction in first 3 months of life; jaundice, progression to cirrhosis

544
Q

What is the pathogenesis of cholelithiasis?

A
  1. supersaturation of cholesterol or bilirubin
  2. decreased phospholipids (lecithin) or bile acids (normally increase solubility)
  3. bile stasis
    - -> precipitation of cholesterol or bilirubin in bile –> stones in gallbladder
545
Q

What are the most common type of gallstones?

A

cholesterol

546
Q

What are the risk factors for development of cholesterol gallstones?

A 
40s
fat
female
fertile (multiple pregnancies, oral contraceptives)
clofibrate
Native American ethnicity
Crohn's disease
CF
cirrhosis
rapid weight loss
547
Q

What are the risk factors for bilirubin/pigment gallstones?

A

increased bilirubin in bile –> extravascular hemolysis
advanced age
Black or Asian
rural population
E. coli biliary infection
Ascaris lumbricoides (infects 25% of the world population, especially in areas of poor sanitation)
Clonorchis sinesis (endemic in China, Korean, Vietnam; also increases risk of cholangitis, cholangiocarcinoma)

548
Q

What are the complications of gallstones (which are normally asymptomatic)?

A 
biliary colic
acute and chronic cholecystitis
ascending cholangitis
gallstone ileus (obstruction of ileocecal valve; fistula develops between gallbladder and small intestine; air seen in biliary tree)
gallbladder cancer
549
Q

How are gallstones diagnosed?

A

ultrasound, radionuclide biliary scan (HIDA)

550
Q

What is Charcot’s triad of cholangitis?

A

jaundice
fever
RUQ pain

551
Q

What is a positive Murphy’s sign? Of what is it indicative?

A

DEFINITION inspiratory arrest on deep RUQ palpation due to pain
INDICATION acute cholecystitis

552
Q

What is biliary colic? What complications may arise?

A

DEFINITION waxing and waning RUQ pain (lasting <4 hours) as stone lodges and dislodges in cystic duct; does NOT present with Murphy’s sign
COMPLICATIONS acute pancreatitis, obstructive jaundice

553
Q

Grossly, how does the gallbladder appear in acute cholecystitis? And in chronic?

A

ACUTE enlarged, tense, red –> green/black
CHRONIC “porcelain gallbladder:” smooth serosa, possibly with subserosal fibrosis; shrunken, hard gallbladder due to dystrophic calcification

554
Q

What differences are there, histologically, between acute and chronic cholecystitis?

A

ACUTE edema, neutrophilic and leukocytic infiltrate, abscess formation, hemorrhage
CHRONIC lymphocytic infiltration, plasma cells, macrophages, fibrosis

555
Q

Other than gallstones, what may cause cholecystitis?

A

ischemic
CMV

NOTE causes other than gallstones are rare

556
Q

Might cholecystitis present with changes in alkaline phosphatase? Why or why not?

A

increased alkaline phosphatase if bile duct becomes involved (seen in acute cholecystitis)

557
Q

What are the complications of acute cholecystitis?

A

dilatation of cystic duct with pressure ischemia
bacterial overgrowth of E. coli (ascending cholangitis)
inflammation
empyema
obstructive jaundice
pancreatitis
RARELY cholecystoenteric fistula, gallstone ileus

558
Q

What is the treatment for acute cholecystitis?

A

cholecystectomy

559
Q

What is Rokitansky-Aschoff sinus?

A

herniation of gallbladder mucosa into the muscular wall, caused by chronic cholecystitis

560
Q

What is the presentation of ascending cholangitis?

A

sepsis (high fever and chills)
jaundice
abdominal pain

561
Q

What is the epidemiology, pathogenesis, presentation, and prognosis of gallbladder carcinoma?

A

EPIDEMIOLOGY elderly women
PATHOGENESIS gallstones –> porcelain gallbladder –> adenocarcinoma arising from glandular epithelium lining gallbladder wall
PRESENTATION cholecystitis
PROGNOSIS poor

562
Q

What is the pathogenesis of acute pancreatitis?

A

alcohol, gallstones&raquo_space; trauma, hypercalcemia, hyperlipidemia, drugs, scorpion stings, mumps, rupture of posterior duodenal ulcer
premature activation of trypsin –> activation of other pancreatic enzymes –> autodigestion of pancreatic parenchyma –> liquefactive hemorrhagic necrosis of pancreas, fat necrosis of peripancreatic fat

563
Q

What is the presentation of acute pancreatitis?

A

SYMPTOMS epigastric abdominal pain radiating to back; nausea and vomiting; periumbilical and flank hemorrhage (necrosis spreads into periumbilical soft tissue and retroperitoneum)
LABS elevated serum lipase (more specific) and amylase; hypocalcemia (consumed during saponification in fat necrosis of the peripancreatic fat; POOR PROGNOSTIC FACTOR)

564
Q

What are the causes of acute pancreatitis?

A 
idiopathic
Genetic: PRSS1, SPINK1, CFTR
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune disease
Scorpion sting
Hypercalcemia/Hypertriglyceridemia (>1000)
ERCP
Drugs (sulfa)
--GET SMASHED--
565
Q

What are the complications of acute pancreatitis?

A

peripancreatic hemorrhage and fluid sequestration –> shock
fibrous, GRANULATION tissue surrounding liquefactive necrosis and pancreatic enzymes –> pancreatic psuedocyst (abdominal mass, most cases non-neoplastic) –> rupture –> release of enzymes into abdominal cavity, hemorrhage
E. coli infection –> pancreatic abscess (abdominal pain, high fever, persistently elevated amylase)
DIC
ARDS
multiorgan failure

566
Q

Are steroids an appropriate treatment for acute pancreatitis?

A

no

567
Q

What is the pathophysiology of chronic pancreatitis?

A

alcohol, cystic fibrosis –> recurrent acute pancreatitis –> fibrosis of pancreatic parenchyma

568
Q

What are the symptoms of chronic pancreatitis?

A

epigastric abdominal pain radiating to back
pancreatic insufficiency –> malabsorption with steatorrhea, fat-soluble vitamin deficiencies
dystrophic calcification of pancreatic parenchyma (“chain of lakes”) due to dilatation of pancreatic ducts
weight loss
clay stools
secondary DM
increased risk for pancreatic carcinoma

NOTE amylase and lipase are elevated, but commonly not useful serologic markers for chronic pancreatitis

569
Q

What are the genetic findings associated with pancreatic adenocarcinoma?

A

K-ras on 12p

p16 CDKN2a on 3p

570
Q

What are the risk factors for pancreatic adenocarcinoma?

A

tobacco use, but not ethanol use
chronic pancreatitis, especially >20 years
age >50 years
Jewish and African-American males

571
Q

What is the presentation of pancreatic carcinoma?

A

epigastric abdominal pain and weight loss
Courvoisier’s sign: obstructive jaundice with pale stools and palpable gallbladder (tumor in head of pancreas)
secondary DM (tumor in body or tail)
pancreatitis
Trousseau syndrome: migratory thrombophlebitis of swelling, erythema, and tenderness in extremities; seen in 10% of patients
elevated CA-19-9, amylase, lipase, and glucose

572
Q

What is the most common location for pancreatic carcinoma?

A

head of the pancreas, causing Courvoisier’s sign of obstructive jaundice

573
Q

I say “Trousseau syndrome,” you say…?

A

cancer, likely pancreatic adenocarcinoma (10% of cases show this symptom)

574
Q

What is the treatment for pancreatic adenocarcinoma?

A

Whipple procedure (en bloc removal of head and neck of pancreas, proximal deuodenum, gallbladder)
chemotherapy
radiation therapy

575
Q

What is the prognosis of pancreatic adenocarcinoma?

A

very poor prognosis normally of 6 months or less, 1 year survival <10%
the cancer is usually already metastasized at presentation

From Flashcardlet (18 decks)

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