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STEP > GI > Flashcards

GI Flashcards

1
Q

ursodiol MOA

A

Nontoxic bile acid. Increases bile secretion + decreases cholesterol secretion and absorption.

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2
Q

ursodiol clinical use

A

PBC + gallstone prevention or dissolution.

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3
Q

Orlistat MOA

A

inhibits gastric and pancreatic lipase, thus leading to decreased breakdown and absorption of dietary fats.

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4
Q

Orlistat AE’s

A

steatorrhea + decreased absorption of fat-soluble vitamins.

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5
Q

metoclopramide MOA

A

D2 receptor antagonist. Increases resting tone, contractility, LES tone, motility. Does not influence colon transport time.

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6
Q

metoclopramide clinical use

A

diabetic and postsurgery gastroparesis, antiemetic

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7
Q

metoclopramide contraindications

A

digoxin + diabetic agents + SBO or Parkinson disease (due to D2 receptor blockade)

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8
Q

metoclopramide AE’s

A

parkinsonian effects, tardive dyskinesia, restlessness, drowsiness, fatigue, depression, diarhea.

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9
Q

ondansetron MOA

A

serotonin antagonist + decreases vagal stimulation

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10
Q

ondansetron AE’s

A

headache + constipation + QT interval prolongation

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11
Q

Loperamide MOA

A

agonist at mu-opioid receptors; slows gut motility. Poor CNS penetration (low addictive potential)

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12
Q

loperamide AE’s

A

constipation + nausea

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13
Q

Sulfasalazine – MOA, clinical use, SE’s

A

Sally Westcott in a sulfur geiser/sulfasalazine. Pyramid with sulfur geiser on top on right + tree with bark and hailing on it/MOA = combination of sulfapyridine (antibacterial) + 5-aminosalicylic acid (anti-inflammatory). Bacteria on counter throwing lasso around her/activated by colonic bacteria. Rachel in wheelchair next to counter/can cause drug-induced lupus. Riding a dead sperm/toxicity = malaise + nausea + sulfonamide toxicity + reversible oligospermia. /clinical use = UC + Crohn disease.

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14
Q

lactulose

A

osmotic laxative

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15
Q

osmotic laxatives AE’s

A

diarrhea, dehydration.

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16
Q

octreotide MOA

A

long-acting somatostatin analog; inhibits secretion of various splanchnic vasodilatory hormones.

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17
Q

Octreotide AE’s

A

nausea, cramps, steatorrhea + increased rick of cholethiasis due to CCK inhibition.

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18
Q

misoprostol MOA

A

PGE1 analog. increased production and secretion of gastric mucous barrier, decreases acid production.

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19
Q

misoprostol mechanism as abortifacent

A

Ripens cervix

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20
Q

Other use of misoprostol.

A

Maintains PDA.

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21
Q

misoprostol AE’s

A

diarrhea

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22
Q

bismuth, sucralfate MOA

A

binds to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer.

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23
Q

another use for bismuth, sucralfate

A

travelers’ diarrhea.

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24
Q

shared AE of all antacids

A

hypokalemia

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25
Q

aluminum hydroxide AE’s

A

constipation + hypophosphatemia + proximal muscle weakness + osteodystrophy + seizures

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26
Q

calcium carbonate AE’s

A

hypercalcemia (milk-alkali syndrome) + rebound acid production

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27
Q

magnesium hydroxide AE’s

A

Harvey milk (sean penn) from movie milk in middle of room giving magnus who’s benchpressing a blowjob: he’s shitting on a towel + IV pole next to him + is being shocked + riding a mini motorcycle/SE’s = diarrhea + hyporeflexia + hypotension + cardiac arrest.

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28
Q

What is a proton pump?

A

H+/K+ ATPase in stomach parietal cells.

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29
Q

ZES treatment

A

PPI

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30
Q

PPI AE’s

A

Nate is banging Heidi on the table + magnus strong man on the table + carson with his ski gear at other end of table/SE’s = increased risk of C. diff infection + decreased serum Mg2+ with long-term use + atrophic gastritis + carcinoid tumors + headaches + GI disturbances. Rest of seats filled with skeletons/associated with osteoporosis and osteoporotic hip fractures (decreases calcium absorption;calcium carbonate requires an acidic environment for proper absorption).

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31
Q

H2 blocker MOA

A

reversible block of histamine H2 receptors –> decreased H+ secretion by parietal cells.

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32
Q

H2 Blocker AE’s

A
  • Cimetidine is the primary concern. Others are relatively free of these effects.
  • CYP450 inhibitor + antiandrogen effects + can cross BBB (confusion, dizziness, headaches) and placenta + decreases renal excretion of creatinine.
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33
Q

ranitidine AE

A

Decreases renal excretion of creatinine.

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34
Q

Foregut region

A

pharynx t oduodenum

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35
Q

midgut region

A

duodenum to proximal 2/3 of transverse colon.

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36
Q

hindgut region

A

distal 1/3 of transverse colon to anal canal above pectinate line.

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37
Q

Midgut development

A

6th week–physiologic midgut herniates through umbilical ring.
10th week–returns to abdominal cavity + rotates around SMA, total 270 counterclockwise.

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38
Q

Defect in rostral fold closure

A

Sternal defects

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39
Q

Defect in lateral fold closure

A

Omphalocele, gastroschisis

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40
Q

defect in caudal fold closure leads to…

A

bladder exstrophy

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41
Q

gastroschisis

A

extrusion of abdominal contents through abdominal folds (typically right of umbilicus); not covered by peritoneum.

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42
Q

Most common tracheoesophageal anomalies

A

esophageal atresia with distal tracheoesophageal fistula (85%)

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43
Q

why does cyanosis occur with esophageal atresia?

A

Secondary to laryngospasm (to avoid reflux-related aspiration).

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44
Q

H-type esophageal atresia

A

Pure TEF. see FA

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45
Q

jejunal and ileal atresia pathophys

A

disruption of mesenteric vessels –> ischemic necrosis –> segmental resoprtion.

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46
Q

characteristic sign of jejunal and ileal atresia.

A

Bowel discontinuity or “apple peel.”

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47
Q

epidemiology of hypertrophic pyloric stenosis

A

Most common cause of gastric outlet obstruction (1:600).

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48
Q

hypertrophic pyloric stenosis RF

A

Exposure to macrolides.

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49
Q

hypertrophic pyloric stenosis acid/base disturbance

A

hypokalemic hypochloremic metabolic alkalosis (vomiting of gastric acid and subsequent volume contraction).

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50
Q

pancreas embryology

A

Derived from foregut. Ventral pancreatic buds contribute to uncinate process and main pancreatic duct. Dorsal pancreatic bud alone becomes body, tail, isthmus, and accessory pancreatic duct. Both ventral and dorsal buds contribut to pancreatic head.

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51
Q

annular pancreas

A

ventral pancreatic bud abnormally encircles 2nd part of duodenum; forming ring of pancreatic tissue that may cause dudoenal narrowing and *nonbilious vomiting.

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52
Q

Pancreas divisum and timeframe

A

Ventral and dorsal parts fail to fuse at 8 weeks. Common and mostly asymptomatic, but may cause chronic abdominal pain and/or pancreatitis.

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53
Q

pancreas anatomy

A

codebook

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54
Q

SADPUCKER notes

A

Aorta AND IVC
2nd-4th parts of duodenum
Pancreas (except tail)
Esophagus (thoracic portion)

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55
Q

falciform connects

A

Liver to anterior abdominal wall

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56
Q

falciform contains

A

ligamentum teres hepatis

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57
Q

ligamentum teres hepatis derived from…

A

fetal umbilical vein

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58
Q

falciform derivative of…

A

ventral mesentery

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59
Q

hepatoduodenal connects…

A

liver to duodenum

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60
Q

hepatoduodenal

A

portal triad

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61
Q

pringle maneuver

A

Compressing hepatoduodenal ligament between thumb and index finger in omental foramen to control bleeding.

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62
Q

hepatoduodenal borders the…

A

omental foramen

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63
Q

omental foramen connnects

A

The greater and lesser sacs.

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64
Q

gastrohepatic connects

A

liver to lesser curvature of stomach

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65
Q

gastrohepatic contains

A
  • gastric arteries

- separates greater and lesser sacs on the right.

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66
Q

what do you need to cut to access the lesser sac?

A

gastrohepatic ligament

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67
Q

gastrocolic connects… forms..

A
  • greater curvature and transverse colon.

- part of greater omentum.

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68
Q

gastrocolic contains

A

gastroepiploic arteries

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69
Q

What separates greater and lesser sacs on the left?

A

gastrosplenic

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70
Q

gastrosplenic connects…forms…

A
  • greater curvature and spleen

- part of greater omentum

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71
Q

gastrosplenic contains

A

short gastrics, left gastroepiploic

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72
Q

splenorenal connects….

A

Spleen to posterior abdominal wall.

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73
Q

Splenorenal contains

A

splenic artery and vein + tail of pancreas

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74
Q

Layers of gut wall

A 
inside to outside -- MSMS
Mucosa
Submucosa
Muscularis externa
Serosa
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75
Q

Mucosa contains…

A

epithelium, lamina propria, muscularis mucosa.

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76
Q

submucosa includes…function..

A
  • Submucosal nerve plexus (Meissner).

- Secretes fluid.

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77
Q

Muscularis externa includes…

A

Myenteric nerve plexus (Auerbach)

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78
Q

serosa caveat

A

Called serosa when intraperitoneal, adventitia when retroperitoneal.

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79
Q

erosions vs. ulcers

A

Ulcers can extend into submucosa, inner or outer muscular layer. Erosions are confined to mucosa.

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80
Q

Stomach basal rhythm

A

3 waves/min

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81
Q

Duodenum basal rhythm

A

12 waves/min

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82
Q

Ileum basal rhythm

A

8-9 waves/min

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83
Q

Muscularis composition

A

Inner circular layer, myenteric nerve plexus (Auerbach), outer longitudinal layer

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84
Q

Brunner glands

A

HCO3- secreting cells of submucosa.

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85
Q

Duodenum contains

A

Brunner glands + cytps of Lieberkuhn + villi and microvilli

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86
Q

histology of jejunum

A

Plicae circularis and crypts of Lieberkuhn.

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87
Q

Peyer patches

A

Lymphoid aggregates in lamina propria, submucosa.

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88
Q

Where are peyer patches?

A

Ileum

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89
Q

Ileum histology

A

peyer patches + plicae circulares + crypts of lieberkuhn.

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90
Q

Where are the largest number of goblet cells in the small intestine?

A

Ileum

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91
Q

Colon histology

A

Crypts of Lieberkuhn but no villi; abundant goblet cells.

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92
Q

abdominal aorta branches rule

A

Arteries supplying GI structures branch anteriorly. Arteries supplying non-GI structures branch laterally and posteriorly.

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93
Q

Middle suprarenal anatomic location.

A

T12

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94
Q

celiac trunk anatomic location.

A

T12

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95
Q

Fist lumbar anatomic location

A

L1

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96
Q

Renal anatomic location

A

L1

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97
Q

SMA anatomic location

A

L1

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98
Q

Gonadal anatomic location

A

Just above L2

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99
Q

IMA anatomic location

A

L3

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100
Q

Bifurcation of abdominal anatomic location

A

L4 (biFOURcation)

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101
Q

Common iliacs anatomic location

A

L5

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102
Q

SMA artery syndrome

1) presentation
2) anatomy
3) scenario

A

1) Intermittent intestinal obstruction symptoms (primarily postprandial pain)
2) Transverse (3rd) portion of duodenum is compressed between SMA and aorta.
3) Conditions associated with diminished mesenteric fat (eg, low body weight/malnutrition).

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103
Q

Foregut

1) arterial supply
2) PS innervation
3) vertebral level
4) structures supplied

A

1) Celiac
2) Vagus
3) T12/L1
4) Pharynx (vagus nerve only) and lower esophagus (celiac artery only) to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)

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104
Q

Midgut

1) arterial supply
2) PS innervation
3) vertebral level
4) structures supplied

A

1) SMA
2) vagus
3) L1
4) distal duodenum to proximal 2/3 of transverse colon

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105
Q

Hindgut

1) arterial supply
2) PS innervation
3) vertebral level
4) structures supplied

A

1) IMA
2) Pelvic
3) L3
4) distal 1/3 transverse colon to upper portion of rectum.

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106
Q

TIPS procedure

A

Transjugular intrahepatic portosystemic shunt (TIPS). Creates a shunt between portal vein and hepatic vein, thus relieving portal HTN by shunting blood to the systemic circulation, bypassing the liver.

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107
Q

Varices seen with portal hypertension

A

(gut, butt, and caput (medusa) –> esophageal, rectal (anorectal varices), caput medusa

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108
Q

portosystemic rectal anastomosis

A

superior rectal with middle and inferior rectal.

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109
Q

caput medusae anastomosis

A

Paraumbilical with small epigastric veins of the anterior abdominal wall.

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110
Q

esophageal varices anastomosis

A

left gastric with azygos

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111
Q

pectinate (dentate) line

A

Formed where endoderm (hindgut) meets ectoderm.

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112
Q

Venous drainage above pecinate line

A

Superior rectal vein –> ifnerior mesenteric –> portal system

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113
Q

lymphatic drainage above pectinate line

A

internal iliac lymph nodes

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114
Q

venous drainage below pectinate line

A

inferior rectal vein –> internal pudendal vein –> internal iliac vein –> common iliac vein –> IVC

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115
Q

lymphatic drainage below pectinate line

A

Superficial inguinal nodes.

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116
Q

Anal fissure RF’s

A

low fiber diet + constipation.

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117
Q

Kupffer cells

A

Specialized macrophages that form the lining of sinusoids

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118
Q

Hepatic stellate (Ito) cells 1) location 2) function

A

1) space of Disse

2) store vitamin A (when quiescent), produce ECM when activated.

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119
Q

intermediate zone, pericentral vein (centrilobular) zone, intermediate zone

A

Zone 1 = periportal zone
Zone 2 = intermediate zone
Zone 3 = pericentral vein (centrilobular) zone

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120
Q

Site of alcoholic hepatitis

A

Zone III

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121
Q

yellow fever affects…

A

zone II

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122
Q

ingested toxins (eg cocaine) affect….

A

Zone I

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123
Q

zone affected 1st by ischemia

A

Zone III (farthest from arterial supply)

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124
Q

zone affected 1st by viral hepatitis

A

Zone I

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125
Q

ampulla of vater and 2) clinical significance

A

1) little widened space behind sphincter of oddi in head of pancreas (FA 347)
2) gallstones that lodge here an block both the common bile and pancreatic ducts causing “double duct sign” –> both cholangitis and pancreatitis.

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126
Q

cystic duct

A

Duct that drains gallbladder

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127
Q

painless juandice

A

pancreatic adenocarcinoma (usually ductal) in head of pancreas that causes of obstruction of common bile duct.

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128
Q

femoral region organization

A

NAVeL –> nerve, artery, vein, lymphatics

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129
Q

femoral triangle

A

contains femoral nerve, artery, vein

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130
Q

femoral sheath

A

fascial tube 3-4 cm below inguinal ligament. Contains femoral vein, artery, and canal (deep inguinal lymph nodes) but NOT femoral nerve.

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131
Q

femoral triangle borders

A
  • superiorly by inguinal ligament.
  • medially by medial border of adductor longus.
  • laterally by medial border of sartorius muscle.
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132
Q

superficial inguinal ring

A

External obie standing in the middle of a golden ring/formed by opening in the external oblique muscle aponeurosis.

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133
Q

Deep inguinal ring

A

• Code: hole down to china beneath trannies/opening in the transversalis fascia.

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134
Q

Layers of inguinal canal

A

Obie Spear on outside, closer to bank with stomach covered in big sperm/external spermatic fascia derived from external oblique. Obie hanging from inside pulling testicles up with a rope/cremasteric muscle and fascia derived from internal oblique. Line of trannies with sperm that have buried into their stomachs/internal spermatic fascia derived from transversalis fascia.

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135
Q

Site of protrusion of direct hernia

A

abdominal wall

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136
Q

Site of protrusion of indirect hernia

A

deep inguinal ring

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137
Q

conjoined tendon

A

formed by transversus abdominis muscle + internal oblique muscle

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138
Q

umbilical hernia defect location

A

defect at linea alba

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139
Q

incarceration

A

hernia that can’t be reduced.

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140
Q

strangulation

A

hernia that becomes ischemic and necrotic

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141
Q

presentation of complicated hernias

A

tenderness, erythema, fever.

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142
Q

structure defective in congenital diaphragmatic hernia and usual location

A
  • pleuroperitoneal membrane.

- left side (no liver for protection)

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143
Q

Site of protrusion of direct inguinal hernia

A

Hesselbach triangle. Bulges directly through abdominal wall.

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144
Q

Other details of direct inguinal hernia

A
  • goes through external (superficial) inguinal ring only.
  • covered by external spermatic fascia.
  • usually in older men.
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145
Q

Femoral hernia epidemiology

A

usually females.

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146
Q

femoral hernia protrusion

A

Below inguinal ligament through femoral canal below and lateral to pubic tubercle.

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147
Q

caveat about femoral hernias

A

More likely to incarcerate or strangulate.

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148
Q

Inguinal (hesselbach) triangle

A

Inferior epigastric vessels, lateral border of rectus abdominis, inguinal ligament

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149
Q

Gastrin source and location

A

G cells (**antrum of stomach, duodenum)

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150
Q

gastrin action

A

increases gastric H+ secretion, growth of gastric mucosa, gastric motility.

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151
Q

gastrin 1) increased by 2) decreased by

A

1) stomach distention/alkalinization, amino acids, peptides, vagal stimulation via gastrin-releasing peptide (GRP)
2) ph

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152
Q

what increases gastrin production?

A

chronic PPI use, chronic atrophic gastritis (H pylori), ZES

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153
Q

Somatostatin source

A

D cells (pancreatic islets, Gi mucosa)

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154
Q

somatostain actions

A

decreases gastric acid and pepsinogen secretion + pancreatic and small intestine fluid secretion + gallbladder contraction + insulin and glucagon release

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155
Q

somatostain regulation

A

increased by acid, decreased by vagal stimulation.

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156
Q

CCK source

A

I cells (duodenum, jejunum)

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157
Q

CCK action

A

Increases pancreatic secretion + gallbladder contraction. Decreases gastric emptying. Increases sphincter of oddi relxation.

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158
Q

CCK regulation

A

Increased by fatty acids, amino acids.

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159
Q

How does CCK cause pancreatic secretion

A

Acts on neural muscarinic pathways.

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160
Q

Secretin source

A

S cells (duodenum)

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161
Q

Secretin actions

A

Increases pancreatic HCO3- secretion + bile secretion. Decreases gastric acid secretion. Functions to neutralize gastric acid in duodenum, allowing pancreatic enzymes to function.

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162
Q

Secretin regulation

A

Increased by acid, fatty acids in lumen of duodenum.

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163
Q

glucose-dependent insulinotropic peptide

A

another name for GIP.

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164
Q

GIP source

A

K cells (duodenum, jejunum)

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165
Q

GIP functions

A

Exocrine: decreases gastric H+ secretion.
Endocrine: increases insulin release.

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166
Q

GIP regulation

A

Increased by fatty acids, amino acids, oral glucose.

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167
Q

Why does oral glucose lead to increased insulin compared to IV

A

GIP secretion.

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168
Q

drug that that acts as a motilin receptor agonist

A

erythromycin

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169
Q

VIP source

A

PS ganglia in sphincters, gallbladder, small intestine

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170
Q

VIP functions

A

Increases intestinal water and electrolyte secretion + increases relaxation of intestinal smooth muscle and sphincters.

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171
Q

VIP regulation

A

Increased by distention and vagal stimulation, decreased by adrenergic input.

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172
Q

Why is there increased LEs tone in achalasia?

A

Loss of NO secretion.

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173
Q

Ghrelin source

A

stomach

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174
Q

Ghrelin clinical relevance

A

Increased in Prader-Willi, decreased after gastric bypass surgery.

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175
Q

gastric acid positive regulators

A

histamine, ACh, gastrin

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176
Q

gastric acid negative regulation

A

somatostatin, GIP, prostaglandin, secretin.

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177
Q

pepsin source and function

A

chief cells, protein digestion

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178
Q

Pepsin regulation

A

increased by vagal stimulation, local acid

179
Q

Bicarbonate source

A 
mucosal cells (stomach, duodenum, salivary glands, pancreas)
brunner glands (duodenum)
180
Q

where does bicarbonate sit?

A

Trapped in mucus that covers the gastric epithelium.

181
Q

How does gastrin increase gastric acid secretion?

A

Indirectly through enterochromaffin-like cells (ECL cells) leading to histamine release rather than through its direct effect on parietal cells.

182
Q

Pancreatic secretions tonicity + flow variance

A

1) isotonic
2) low flow –> high Cl-
high flow –> high HCO3-

183
Q

alpha-amylase caveat

A

secreted in active form. Doesn’t need to be activated.

184
Q

name some proteases

A

trypsin, chymotrypsin, elastase, carboxypeptidase.

185
Q

How is trypsinogen converted to trypsin?

A

Enterokinase/enteropeptidase, a brush-border enzyme on duodenal and jejunal mucosa.

186
Q

Glucose and galactose absorption

A

Taken up by SGLTI (Na+ dependent).

187
Q

Fructose absorption

A

Facilitated diffusion by GLUT-5.

188
Q

GLUT 2 function

A

transports all monosaccharides (glucose, galactose, and fructose) to blood.

189
Q

Functon of D-xylose absorption test

A

Distinguishes GI mucosal damage from other causes of malabsorption.

190
Q

B12 absorption caveat

A

absorbed with bile salts.

191
Q

peyer patch and location

A

unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum.

192
Q

Where do IgA-secreting plasma cells sit? What are they derived from

A

Lamina propria. Derived from B cells when stimulated in germinal centers.

193
Q

Composition of bile salts

A

Bile acids conjugated to glycine or taurine, making them water soluble.

194
Q

Composition of bile

A

Bile salts + phospholipids + cholesterol + bilirubin + water + ions.

195
Q

Enzyme catalyzing rate-limiting step of bile acid synthesis.

A

Cholesterol 7alpha-hydroxylase.

196
Q

Bile functions

A

1) Digestion and absorption of lipids and fat-soluble vitamins.
2) Cholesterol excretion (body’s only means of eliminating cholesterol)
3) Antimicrobial activity (via membrane disruption).

197
Q

Bilirubin cycle

A

Heme is metabolized by heme oxygenase to biliverdin –> biliverdin reduced to bilirubin –> unconjugated bilirubin is removed from blood by liver, conjugated with glucuronate, and excreted in bile –> gut bacteria metabolize conjugated bilirubin to urobilinogen –> 80% of urobilinogen is excreted in feces as sercobilin (brown color of stool). 20% of urobilinogen remains in gut. Of that 20%, 10% goes to kidney and is excreted in urine as urobilin (giving urine yellow color) and 90% goes back through enterohepatic circulation to the liver.

198
Q

Direct bilirubin

A

conjugated with glucuronic acid; water soluble.

199
Q

Indirect bilirubin

A

Unconjugated; water insoluble.

200
Q

Where does initial part of bilirubin cycle occur?

A

RBCS –> heme –> unconjugated bilirubin occurs in macrophages.

201
Q

enzymes that conjugates bilirubin

A

UDP-glucuronosyl-transfease.

202
Q

Benign/malignant pattern of salivary gland tumors.

A

Most commonly benign and in parotid gland. Tumors in smaller glands more likely malignant.

203
Q

Typical presentation of salivary gland tumor

A

Painless mass/swelling.

204
Q

What does facial pain or paralysis in a salivary gland mass suggest?

A

Malignant involvement of CN VII.

205
Q

Most common salivary gland tumor

A

Pleomorphic adenoma

206
Q

Pleomorphic adenoma characteristics and composition

A

Benign mixed tumor. Composed of chondromyxoid stroma and epithelium and recurs if incompletely excised or ruptured intraoperatively.

207
Q

Most common malignant salivary gland tumor

A

mucoepidermoid carcinoma.

208
Q

Another name for Warthin tumor

A

Papillary cystadenoma lymphomatosum.

209
Q

Warthin tumor

A

Benign cystic tumor with germinal centers.

210
Q

Causes of secondary achalasia

A

1) chagas disease 2) extraesophageal malignancies (mass effect or paraneoplastic)

211
Q

Barium swallow finding of achalasia

A

birds break

212
Q

achalasia characteristics

A

Failure of relaxation of LES due to loss of myenteric (Auerbach) plexus. High LES resting pressure and uncoordinated or absent peristalsis, leading to progressive dysphagia to solids and liquids.

213
Q

Obstructive dysphagia presentation vs. achalasia

A

Obstructive dysphagia only occurs with solids, achalasia occurs with both liquids and solids.

214
Q

Endoscopy findings in eosinophilic esophagitis

A

Esophageal rings and linear furrows.

215
Q

patient presenting with GERD but unresponsive to GERD therapy consider…

A

eosinophilic esophagitis

216
Q

Pathophys of food impaction in eosinophilic esophagitis

A

Food allergens –> dysphagia –> food impaction.

217
Q

What causes esophageal strictures?

A

1) Caustic ingestion

2) Acid reflux

218
Q

esophageal varices

A

dilated submucosal veins in lower 1/3 of esophagus secondary to portal HTN.

219
Q

atypical but common presentation of GERD

A

cough + hoarseness (laryngopharyngeal reflux).

220
Q

GERD association

221
Q

Plummer-Vinson triad

A

dysphagia + iron deficiency anemia + esophageal webs

222
Q

plummer vinson association

223
Q

sclerodermal esophageal dystomility pathophys

A

esophageal smooth muscle atrophy –> decreased LES pressure and dysmotility –> acid reflux and dysphagia –> stricture, Barrett esophagus, and aspiration.

224
Q

Barrett’s cancer association

A

ADENOCARCINOMA

225
Q

more common esophageal cancer worldwide

A

squamous cell carcinoma

226
Q

RF’s for esophageal adenocarcinoma

A

Chronic GERD, barrett’s, obesity, smoking, achalasia

227
Q

part of esophagus affected in squamous vs. adeno

A

Upper 2/3 = SCC

Lower 1/3 = adeno

228
Q

prostaglandin affected by NSAIDs

229
Q

Curling ulcers

A

Complications from severe burns. (burned by the curling iron)

230
Q

Curling ulcer pathophys

A

hypovolemia –> mucosal ischemia.

231
Q

Cushing ulcer

A

Ulcer resulting from brain injury (cushin the brain)

232
Q

Cushing ulcer pathophys

A

Brain injury –> increased vagal stimulation –> increased ACh –> increased H+ production.

233
Q

Chronic gastritis pathophys

A

Mucosal inflammation, leads to atrophy (hypochlorhydria –> hypergastrinemia) and intestinal metaplasia.

234
Q

H pylori cancer association

A

MALT lymphoma

235
Q

H pylori location

A

affects antrum first, then spreads to body of stomach.

236
Q

autoimmune gastritis location of damage

A

body/fundus of stomach

237
Q

menetrier benign/malignant?

A

precancerous

238
Q

gastric cancer epidemiology

A

Gastric adenocarcinoma –> lymphoma –> GI stromal tumor –> carcinoid (rare).

239
Q

Gastric cancer personality + presentation

A

Early aggressive local spread with node/liver metastases. Often presents late with weight loss + early satiety, acanthosis nigricans, leser-trelat.

240
Q

Intestinal gastric cancer associations

A

H pylori, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, chronic gastritis.

241
Q

Intestinal gastric cancer location + what it looks like

A

Lesser curvature; looks like ulcer with raised margins.

242
Q

Diffuse gastric cancer associations

A

NOT associated with H pylori. Signet ring cells; stomach wall grossly thickened and leathery (linitis plastica)

243
Q

Krukenberg tumor histology

A

Abundnat mucin-secreting, signet ring cells.

244
Q

Gastric ulcer pain vs. duodenal ulcer pain

A

Gastric, Greater with meals. Duodenal decreases with meals.

245
Q

H pylori association with gastric or duodenal ulcers

A

Causes pretty much all duodenal ulcers and 70% of gastric ulcers.

246
Q

Gastric ulcer management

A

Biopsy margins to rule out malignancy

247
Q

Gastric ulcer benign/malignant?

A

Increased risk of carcinoma

248
Q

Gastric ulcer mechanism

A

decreased mucosal protection against gastric acid.

249
Q

Duodenal ulcer mechanism

A

decreased mucosal protection OR increased gastric acdi secretion

250
Q

Other causes of duodenal ulcrs

251
Q

duodenal ulcer – benign/malignant?

A

Usually benign.

252
Q

Duodenal ulcer association

A

hypertrophy of brunner glands

253
Q

duodenal area prone to hemorrhaging

A

posterior more common than anterior.

254
Q

Most common complication of ulcers

A

hemorrhaging

255
Q

Artery associated with ruptured gastric ulcer on lesser curvature of stomach

A

left gastric

256
Q

Artery associated with hemorrhaging ulcer on posterior wall of duodenum

A

gastroduodenal

257
Q

Potential ulcer complications

A

1) hemorrhaging
2) obstruction (pyloric channel, duodenal)
3) perforation.

258
Q

Area of duodenum prone to perforation.

A

anterior>posterior.

259
Q

Free air under diaphragm with referred pain to shoulder via phrenic nerve….

A

perforated duodenum from duodenal ulcers.

260
Q

cancer and celiac’s?

A

moderately increased risk of T-cell lymphoma

261
Q

histo findings in celiac’s

A

villous atrophy + crypt hyperplasia + **intraepithelial lymphocytosis.

262
Q

area primarily affected by celiac’s

A

mucosal absorption decreased in distal duodenum and/or proximal jejunum.

263
Q

Test for celiacs

A

1) serology for antibodies

2) d-xylose for malabsorption

264
Q

d-xylose results

A

1) if blood and urine levels are decreased –> mucosal defect or bacterial overgrowth
2) if pancreatic insufficiency, then will be normal.

265
Q

Material that accumulates in clear cell carcinoma

A

high in glycogen and lipids

266
Q

lactose intolerance diagnosis + analyzing results

A

lactose hydrogen breath test. Positive for lactose malabsorption if postlactose breath hydrogen value rises > 20 ppm compared with baseline.

267
Q

Thing to remember about pancreatic insufficiency

A

not only malabsorption of fat-soluble vitamins but also B12

268
Q

Pancreatic insufficiency diagnosis

A

Decreased duodenal pH (bicarbonate) and fecal elastase.

269
Q

region of intestine affected in tropical sprue

A

Duodenum + jejunum but can involve ileum.

270
Q

anemia relationship to tropical sprue

A

due to folate deficiency, and, later, B12 deficiency.

271
Q

ulcers in chrohn’s

A

linear ulcers

272
Q

microscopic morphology in crohn’s

A

noncaseating granulomas + lymphoid aggregates.

273
Q

Other complications of Crohn’s

A

1) enterovesical fistula, which can cause recurrent UTI and pneumaturia.
2) phlegmon/abscess
3) strictures (causing obstruction)
4) perianal disease.
5) kidney stones
6) gallstones

274
Q

antibiotics for Crohn’s patients

A

Ciprofloxacin + metronidazole

275
Q

UC gross morphology

A

1) Mucosal and submucosal inflammation only.
2) Friable mucosal pseudopolyps with freely hanging mesentery.
3) Loss of haustra –> “lead pipe” appearance on imaging

276
Q

Complications of UC

A

1) Fulminant colitis
2) Toxic megacolon
3) Perforation

277
Q

Primary sclerosing cholangitis lab finding

278
Q

UC treatment

A

5-aminosalicylic preparations (eg, mesalamine), 6-mercaptopurine, infliximab, colectomy.

279
Q

IBS presentatoin

A

Recurrent abdominal pain associated with 2 of following

1) pain improves with defecation
2) change in stool frequency
3) change in appearance of stool.
- - can be diarrhea-predominant or constipation-predominant or mixed.

280
Q

appendicitis pathophys

A

In adults –> obstruction by fecalith.

In kids –> lymphoid hyperplasia.

281
Q

Test for appendicitis and location

A
  • McBurney point

- 1/3 the distance from right anterior superior iliac spine to umbilicus.

282
Q

Other signs in appendicits

A

Psoas, obturator, Rovsing signs. guarding and rebound tenderness on exam.

283
Q

appendicitis differential

A

diverticulitis (elderly), ectopic, yersinia

284
Q

Most common site of diverticulum

A

Sigmoid colon

285
Q

What does “false” mean in relation to diverticulum?

A

Attenuated muscularis externa. Only mucosa and submucosa outpouch.

286
Q

True diverticulum

A

all 3 gut wall layers, Meckels

287
Q

Area prone to false diverticula

A

Where vasa recta perforate muscularis externa.

288
Q

diverticulosis

A

Many false diverticula of the colon, commonly sigmoid.

289
Q

epidemiology of diverticulosis

A

1/2 of people over age 60.

290
Q

diverticulosis pathophys

A

Increased intraluminal pressure and focal weakness in colonic wall. Low-fiber diets.

291
Q

Painless bleeding in a person with diverticulosis

A

Painless hematochezia. *not necessarily diverticulitis.

292
Q

diverticulitis

A

Diverticulosis with inflamed microperforations.

293
Q

Presentation of diverticulitis

A

LLQ pain + fever + leukocytosis.

294
Q

Diverticulitis treatment

A

antibiotics

295
Q

Complications of diverticulitis

A

1) abscess
2) fistula (colovesical fistula leading to pneumaturia)
3) obstruction (inflammatory stenosis)
4) perforation (leading to peritonitis)

296
Q

If diverticulitis is complicated, management is…

A

Percutaneous drainage or surgery.

297
Q

Where does mucosal tissue herniate in Zenker’s?

A

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

298
Q

Meckel presentation

A

melena + RLQ pain.

299
Q

Meckel complications

A

intussusception + volvulus + obstruction near terminal ileum.

300
Q

omphalomesenteric cyst

A

Cystic dilation of vitelline duct. Not peristence of vitelline duct.

301
Q

Six 2’s of Meckel’s

A 
2x as likely in males
2 inches long
2 feet from ileocecal valve
2% of population
presents in first 2 years of life
2 types of epithelia (gastric/pancreatic).
302
Q

Hirschsprung etiology

A

Congenital megacolon characterized by lack of ganglion cells/enteric nervous plexuses (Auerbach and Meissner plexuses) in distal segment of colon.

303
Q

Hirschprung genetic association

A

mutations in RET

304
Q

Hirschsprung presentation

A

Bilious emesis + abdominal distention + failure to pass meconium within 48 hours –> chronic constipation.

305
Q

Hirschsprung diagnosis

A

Rectal suction biopsy

306
Q

Hirschsprung treatment

307
Q

Positioning of bowel in malrotation

A

small intestine in ball in bottom right, large intestine on left side, ladd band between large intestine and liver.

308
Q

Complications of malrotation

A

1) volvulus

2) duodenal obstruction

309
Q

intussusception

A

PROXIMAL segment telescopes into distal segment.

310
Q

viral infection and intussusception etiology

A

adenovirus –> peyer patch hypertrophy –> lead point.

311
Q

Most common pathologic lead point

A

Meckel diverticulum.

312
Q

Usual location of acute mesenteric ischemia

A

Embolic occlusion of SMA.

313
Q

chronic mesenteric ischemia pathophys

A

“intestinal angina”: atherosclerosis of celiac, IMA, or SMA –> intestinal hypoperfusion –> postprandial epigastric pain –> food aversion and weight loss.

314
Q

colonic ischemia presentation

A

crampy abdominal pain followed by hematochezia.

315
Q

Watershed areas

A

splenic flexure, distal colon.

316
Q

Most common locations of angiodysplasia

A

Cecum, terminal ileum, ascending colon.

317
Q

Most common cause of SBO

318
Q

Adhesion presentation

A

Fibrous band of scar tissue. Can have well-demarcated necrotic zones.

319
Q

Ileus

A

Intestinal hypomotility without obstruction –> constipation and decreased flatus; distended/tympanic abdomen with decreased bowel sounds.

320
Q

Ileus causes

A

abdominal surgeries, opiates, hypokalemia, sepsis.

321
Q

ileus treatment

A

Bowel rest, electrolyte correction, cholinergic drugs (stimulate intestinal motility).

322
Q

necrotizing enterocolitis pathophys

A

formula fed premies –> immature immune system –> necrosis of intestinal mucosa (primarily colonic) with possible perforation, which can lead to pneumatosis intestinalis, free air in abdomen, portal venous gas.

323
Q

What induces COX-2 production?

324
Q

Inguinal (hesselbach) triangle borders

A

Inferior epigastric vessels, lateral border of rectus. abdominis, inguinal ligament

325
Q

hyperplastic polyp location and presentation

A

non-neoplastic and smaller. Rectosigmoid area.

326
Q

hamartomatous polyps histology

A

growths of normal colonic tissue with distorted architecture.

327
Q

adenomatous polyps + presentation

A

neoplastic, via chromosomal instability pathway. APC and KRAS mutations.
Usually asymptomatic; may present with occult bleeding.

328
Q

serrated polyps

1) genetics
2) epidemiology

A

1) premalignant via CPG hypermethylation phenotype pathway with microsatelite instability and mutations in BRAF.
2) Up to 20% of cases of sporadic CRC.

329
Q

2 hit hypothesis

A

You need to lose 2 tumor suppressor genes before getting cancer.

330
Q

Gardner syndrome

A

FAP + osseus and soft tissue tumors + congenital hypertrophy of retinal pigment epithelium + impacted/supernumerary teeth.

331
Q

Peutz Jeghers syndrome

A

o Coded character: Megan Yeiter. Emerging from jegher bag in basement with hyperpigmented mouth, lips, genitalia and covered in ham/syndrome featuring numerous hamartomas throughout GI tract. /presentation = hyperpigmented mouth/lips/hands/genitalia + bloody stool (due to intestinal hamartomas). Kenny sitting to her left + Mr. Kolkhorst sitting on a toilet behind her + tammy on her right + T with gut next to kenny/associated with increased risk of colorectal, breast, stomach, small bowel, and pancreatic cancers (but hamartomas themselves don’t undergo malignant transformation) + ovary/uterus/cervix/lung. Femdom chick whipping her from right /autosomal dominant. /pedunculated polyps. Intussuscepted bowel hanging over her from left/hamartomas can occasionally serve as the lead point for intussusception.

332
Q

Peutz jeghers mutation

A

STK11/LKB1 gene.

333
Q

Juvenile polyposis syndrome

1) presentation
2) prognosis

A
  • AD syndrome in children less than 5 featuring numerous hamartomatous polyps in colon, stomach, small bowel.
  • increased risk of CRC
334
Q

Epidemiology of cancer progression in lynch syndrome + area of involvement

A

80% progress to CRC + proximal colon is always involved.

335
Q

Cancers associated with Lynch syndrome

A

Associated with endometrial, ovarian, and skin cancers.

336
Q

genetics of CRC

A

25% have a family history.

337
Q

CRC RF’s

A

1) adenomatous and serrated polyps
2) familial cancer syndromes
3) IBD
4) tobacco use
5) diet of processed meat with low fiber.

338
Q

Areas most commonly involved in CRC

A

Rectosigmoid>ascending>descending

339
Q

Ascending mass in CRC presentation

A

exophytic mass + IDA + weight loss

340
Q

descending mass in CRC presentation

A

Infiltrating mass, partial obstruction, colicky pain, hematochezia.

341
Q

Caveat about CEA tumor marker for CRC

A

Good for monitoring recurrence, shouldn’t be used for screening.

342
Q

Screening for CRC

A

Colonoscopy, flexible sigmoidoscopy, fecal occult blood test, or fecal DNA test.

343
Q

Genetic cause of most sporadic CRC

A

Mutations in APC

344
Q

Mismatch repair gene

345
Q

Chromosomal instability pathway for CRC

A

APC –> KRAS –> p53, DCC

346
Q

Cells responsible for fibrosis in cirrhosis

A

Stellate cells

347
Q

histology of fibrosis

A

diffuse bridging fibrosis + regenerative nodules.

348
Q

Causes of portal HTN

A

cirrhosis + vascular obstruction (Budd-Chiari) + schisto

349
Q

metabolic presentation of cirrhosis and portal HTN

A

cardiomyopathy + peripheral edema

350
Q

hematologic presentation of cirrhosis and portal HTN

A

thrombocytopenia + anemia + coagulation disorders

351
Q

fetor hepaticus

A

“breath of the dead.” Late sign of liver failure and feature of hepatic encephalopathy. Breath has a sweet, fecal smell to it.

352
Q

Reproductive presentation of cirrhosis and portal HTN

A

testicular atrophy + gynecomastia + amenorrhea

353
Q

What does AST greater than ALT in nonalcoholic liver disease suggest…

A

progression to advanced fibrosis or cirrhosis.

354
Q

ALT, AST pattern in most liver disease

A

ALT is greater than AST, alcoholic liver disease is the exception

355
Q

Marker of cholestasis

356
Q

gamma-glutamyl transpeptidase

A

increased in various liver and biliary disease, but not in bone disease.

357
Q

Albumin as a marker of liver disease

A

decreased in advanced liver disease

358
Q

Prothrombin as a marker of liver disease

A

Increased in advanced liver disease (decreased production of clotting factors)

359
Q

Platelets as a marker of liver disease

A

decreased in advanced liver disease

360
Q

Why are platelets decreased in advanced liver disease?

A

decreased thrombopoietin, liver sequestration and portal HTN (splenomegaly/splenic sequestration).

361
Q

viral infections associated with Reye syndrome

A

VZV + influenza B

362
Q

Reye syndrome pathophys

A

aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzymes.

363
Q

alcoholic hepatitis histology

A

swollen and necrotic hepatocytes with neutrophilic infiltration.

364
Q

Mallory bodies

A

intracytoplasmic eosinophilic inclusions of damaged keratin filaments.

365
Q

alcoholic cirrhosis histology

A

Micornodular, irregularly shrunken liver with “hobnail” appearance. Sclerosis around central vein.

366
Q

Non alcoholic fatty liver disease:

A

Super fat hippos sitting around perimeter + inflating balloons + grim reaper sitting in middle/metabolic syndrome (insulin resistance) fatty infiltration of hepatocytes “cellular ballooning” and eventual necrosis. Ollie sitting in chair holding fetus in front of grim reaper/may cause cirrhosis and HCC. /independent of alcohol use. Huge alan + tiny Trojan Spartan to his right/ALT>AST.

367
Q

antibiotic treatment for hepatic encephalopathy

A

rifaximin or neomycin

368
Q

hepatic encephalopathy trigers

A

1) increased NH3 production and absorption (due to dietary protein, GI bleed, constipation, infection).
2) decreased NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS).

369
Q

lactulose MOA in hepatic encephalopathy

A

Decreases intraluminal ammonia absorption. Lactulose is metabolized by gut bacteria into lactic and acetic acid. The H+ ions emitted bind to NH3, converting it into NH4+ and thereby preventing it’s absorption. Thus, increase NH4+ generation.

370
Q

alpha1-antitrypsin deficiency cancer association

371
Q

cavernous hemangioma prognosis

372
Q

hepatic adenoma prognosis

A

May regress spontaneously or rupture (abdominal pain and shock

373
Q

Most common liver tumor mets

A

GI + breast + lung

374
Q

budd-chiari associations

A

hypercoagulable states + polycythemia vera + postpartum state + HCC

375
Q

caveat aboud Budd-chiari

A

Absence of JVD.

376
Q

pathophys of alpha1-antitrypsin deficiency in liver

A

Misfolded gene product protein aggregates in hepatocellular ER, causing cirrhosis with PAS positive globules in liver.

377
Q

hyperbilirubinemia associated with primary sclerosing cholangitis

A

conjugated

378
Q

hyperbilirubinemia associated with PBC

A

conjugated

379
Q

Mixed (direct and indirect hyperbilirubinemia) seen in…

A

hepatitits, cirrhosis

380
Q

physiologic neonatal jaundice prognosis

A

usually resolves without treatment in 1-2 weeks.

381
Q

phototherapy for neonatal jaundice mechanize

A

Isomerizes unconjugated bilirubin to water-soluble form

382
Q

hereditary hyperbilirubinemias genetics

383
Q

Gilbert syndrome mechanism

A

Mildly decreased UDP-glucoronysltransferase conjugation and impaired bilirubin uptake.

384
Q

Treatment for Crigler-Najjar type I

A

Plasmapheresis and phototherapy

385
Q

Type II Crigler-Najjar

A

Less severe and responds to phenobarbital, which increases liver enzyme synthesis.

386
Q

Rotor syndrome etiology

A

Impaired hepatic uptake and excretion.

387
Q

another name for conjugated bilirubin

A

bilirubin diglucuronide

388
Q

another name for Wilson’s

A

hepatolenticular degeneration

389
Q

gene mutation in Wilson’s

390
Q

labs in Wilson’s

A

DECREASED ceruloplasmin

391
Q

Kaysr-Fleischer rings

A

deposits in Descemet membrane of cornea

392
Q

Wilson’s treatment

A

chelation with penicillamine or trientine, oral zinc.

393
Q

HFE chromosome

394
Q

hemochromatosis

  • ferritin
  • TIBC
  • transferrin
A

Increased ferritin, increased iron, decreased TIBC, increased transferrin saturation.

395
Q

Iron overload also seen in..

A

chronic transfusion therapy (beta-thalassemia major)

396
Q

hemochromatosis presentation

A

Presents after age 40 when total body iron > 20 g.

397
Q

cardiac presentation of hemochromatosis

A

dilated cardiomyopathy (reversible)

398
Q

hemochromatosis treatment

A

Repeated phlebotomy, chleation with deferasirox, deferoxamine, oral deferiprone.

399
Q

cholestatic pattern of LFTs (characteristic of biliary tract disease)

A

Increased conjugated bilirubin, increased cholesterol, increased ALP.

400
Q

Lab findings in PSC

A
  • p-ANCA positive

- increased IgM

401
Q

PSC complications

A

1) biliary cirhosis

2) increased risk of cholangiocarcinoma and gallbladder cancer.

402
Q

Secondary biliary cirrhosis 1) pathophys

A

1)Extrahepatic biliary obstruction leads to increased pressure in intrahepatic ducts, leading to injury/fibrosis and bile stasis.

403
Q

Secondary biliary cirrhosis epidemiology

A

Patients with known obstructive lesions (gallstones, biliary strictures, pancreatic carcinoma)

404
Q

Secondary biliary cirrhosis complication

A

Ascending cholangitis

405
Q

what causes gallstones

A

increased cholesterol and/or bilirubin, decreased bile salts, and stasis.

406
Q

cholesterol gallstone associations

A

Obestity, crohns, advanced age, estrogen therapy, multiparity, rapid weight loss, Native American.

407
Q

black pigment stone composition

A

Calcium bilirubinate

408
Q

Brown pigment stone etiology

409
Q

pigment stone associations

A

Crohn’s, advanced age, chronic hemolysis, alcoholic cirrhosis, biliary infections, total parenteral nutrition.

410
Q

complications of gallstones

A

1) cholecystitis
2) acute pancreatitis
3) ascending cholangitis
4) fistula between gallbladder and GI tract (air in biliary tree0

411
Q

charcot triad of cholangitis

A

Jaundice + fever + RUQ pain

412
Q

pneumobilia

A

air in biliary tree

413
Q

gallstone ileus

A

osbtruction of ileocecal valve due to gallstone from fistula

414
Q

Increased ALP suggests

A

bile duct involvement (ascending cholangitis)

415
Q

cholecystitis diagnosis

A

US or cholescintigraphy (HIDA, or hepatobiliary iminiodiacetic acid scan).

416
Q

causes of alcalculous cholecystitis

A

ischemia and stasis or CMV

417
Q

causes of acute pancreatitis

A

I GET SMASHED. Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hypertriglyceridemia (>1000 mg/dL), ERCP, Drugs (sulfa drugs, NRTIs, protease inhibitors).

418
Q

acute pancreatitis diagnosis

A

2/3 criteria: acute epigastric pain often radiating to the back, increased serum amylase or lipase (more specific) to 3x upper limit of normal, or characteristic imaging findings.

419
Q

another complication of acute pancreatitis

A

hypocalcemia (precipitation of Ca2+ soaps)

420
Q

chronic pancreatitis

A

Chronic inflammation, atrophy, calcification of the pancreas.

421
Q

chronic pancreatitis caveat

A

amylase and lipase may or may not be elevated (almost always elevated in acute pancreatitis)

422
Q

pancreatic adenocarcinoma personality

A

Often metastatic at presentation with average survival around 1 year.

423
Q

Trousseau syndrome

A

migratory thrombophlebitis

424
Q

Courvoisier sign

A

palpable, nontender gallbladder, characteristic of pancreatic adenocarcinoma.

425
Q

Treatment for pancreatic adenocarcinoma

A

Whipple procedure + chemo + radiation.

426
Q

gastrin pathway

427
Q

somatostatin pathway

428
Q

Prostaglandin pathway

429
Q

alkaline tide

A

increased blood pH after gastric acid secretion (eg, after meals, vomiting)

430
Q

carbonic anhydrase

A

interconverts CO2 + H2 H2CO3

431
Q

How is Cl excreted in parietal cells

A

HCO3-/Cl- exchanger generates Cl- gradient, then diffuses through channels out

432
Q

Gastrin receptor on parietal cells

433
Q

ACh receptor on parietal cells

434
Q

Cholera mechanism

A

He’s on a stationary bike + there’s tents set up all over the room + swat team is breaking into his house/cholera A-B toxin (a for activating, b for binding) activates adenyl cyclase by ADP ribosylation to increase cAMP. *This leads to increased Cl- secretory channels in crypt cells.

435
Q

CCK has some gastrin-like properties because both CCK and gastrin

A

Have 5 identical C-terminal amino acids.

436
Q

Monosaccharide transport caveat

A

Fructose is the only monosaccharide that that is not absorbed by Na+-dependent cotransport. It it stransported by facilitated diffusion.

437
Q

Amino acid absorption in the intestine

A

Na+-dependent cotransport (*except for oligopeptides)

438
Q

Fatty acid absorption

A

simple diffusion

439
Q

Why does ileal resection (such as for Crohn’s patients) cause steatorrhea?

A

Ileum normally transports bile acids from the lumen of the gut. Thus, with ileal resection new synthesis of bile acids is needed to replace bile acids that are lost in the feces. With ileal resection most of bile acids secreted are excreted in the feces and the liver pool is diminished. ***Bile acids are needed for micelle formation in the intestinal lumen to solubilize products of lipid digestion so that they can be absorbed. So the problem is MICELLES DO NOT FORM in the intestinal lumen.

440
Q

Where are chylomicrons formed?

A

Within intestinal epithelial cells and are transported to lymph vessels.

441
Q

Function of CCK

A

Mediates digestion in the small intestine by inhibiting gastric emptying and decreasing gastric acid secretion. Lines small intestine.

442
Q

Saliva characteristics

A

1) hypotonic
2) high HCO3- concentration
3) alpha-amylase and lingual lipase

443
Q

control of saliva production

A

Parasympathetic, thus it is abolished by vagotomy.

444
Q

What are slow waves in small intestinal smooth muscle cells?

A

oscillating resting membrane potentials.

STEP (85 decks)

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