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FirstAID > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Retroperitoneal structures:

A

“SAD PUCKER”

  • Suprarenal (adrenal) gland
  • Aorta and IVC
  • Duodenum (2nd, 3rd, and 4th parts)
  • Pancreas (except tail)
  • Ureters
  • Colon (descending and ascending)
  • Kidneys
  • Esophagus (lower 2/3)
  • Rectum (upper 2/3)
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2
Q

GI ligament that is a derivative of the fetal umbilical vein? what structure does it contain? what does it connect?

A

Falciform ligament

  • contains the ligamentum teres
  • derivative of the fetal umbilical vein
  • connects liver to anterior abdominal wall
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3
Q

GI ligament that contains the portal triad (hepatic artery, portal vein, common bile duct)?

A

Hepatoduodenal ligament

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4
Q

Which GI ligament may be compressed to control bleeding by placing fingers in the omental foramen?

A

Hepatoduodenal ligamentf

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5
Q

Frequency of waves/peristalsis in stomach? duodenum? ileum?

A

stomach–> 3 waves/min
duodenum–> 12 waves/min
ileum–> 8-9 waves/min

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6
Q

Meissner’s plexus:

  • where’s it located?
  • other name?
  • what’s its function?
A
  • located in Submucosa
  • “submucosal plexus”
  • controls secretory activity; secretes mucus (so is near the lumen…)
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7
Q

Auerbach’s plexus:

  • where’s it located?
  • other name?
  • what’s its function?
A
  • located in Musculara externa (really, between muscularis externa inner circular and outer longitudinal layers)
  • “Myenteric plexus”
  • controls muscle contractions; coordinates motility along entire gut wall
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8
Q

Roles of the mucosa of the GI tract?

A

mucosa = innermost layer of gut wall

  • has 3 parts, each with a role:
  • epithelium–> absorption
  • lamina propria–> support
  • muscularis mucosa–> motility
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9
Q

cell type in esophagus?

A

stratified squamous epithelium

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10
Q

cell type in stomach?

A

gastric glands

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11
Q

where in GIT are Brunner’s glands?

A

Duodenum

–>submucosal glands that produce alkaline-rich/bicarb secretion

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12
Q

Where in GIT are Crypts of Lieberkuhn?

A

Duodenum, Jejunum, Ileum, and Colon

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13
Q

Where in GIT are villi and microvilli?

A

Small intestine; not Colon (makes sense, b/c villi are there to increase absorptive surface)

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14
Q

Where in GIT are goblet cells?

A

Ileum–> has most goblet cells in the small intestine; but, also found in other parts of small intestine: as go along the small intestine, # of goblet cells increases

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15
Q

Where in GIT are Peyer’s patches?

A

only in Ileum

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16
Q

Where does celiac trunk come off the abdominal aorta?

A

T12

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17
Q

Where does the SMA come off the abdominal aorta?

A

L1

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18
Q

Where do the renal arteries come off the abdominal aorta?

A

L1

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19
Q

Where does the inferior mesenteric artery come off the abdominal aorta?

A

L3

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20
Q

What level is the bifurcation of the abdominal aorta?

A

L4

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21
Q

Muscle types composing the Esophagus:

A
  • upper 3rd–> striated muscle (voluntary)
  • middle 3rd–> striated + smooth muscle
  • lower 3rd–> smooth muscle (involuntary)
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22
Q

Artery that supplies the Foregut? Innervation of the foregut?

A
  • Celiac artery

- Vagus nerve

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23
Q

Artery and Nerve that supply the Midgut?

A
  • SMA

- Vagus nerve

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24
Q

Artery and Nerve that supply the hindgut?

A
  • IMA

- Pelvic nerve

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25
Q

Watershed area of the GIT?

A

=> splenic flexure

-supplied by the terminal branches of the IMA and SMA, so most sensitive to hypoxia

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26
Q

What structures make up the foregut? midgut? hindgut?

A
  • foregut: stomach to proximal duodenum; also: liver, gallbladder, pancreas, spleen
  • midgut: Distal duodenum to proximal 2/3 of transverse colon
  • hindgut: distal 1/3 or transverse colon to upper part of rectum; inludes splenic flexure (watershed area)
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27
Q

Portal triad:

A
  • Hepatic artery
  • Portal vein
  • Common bile duct
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28
Q

Branches of celiac trunk?

A
  • celiac trunk comes off abdominal aorta at T12
  • branches:
  • common hepatic artery
  • splenic artery
  • left gastric artery

–> these branches make up the main blood supply of the stomach!

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29
Q

Which arteries supply the lesser curvature of the stomach? greater curvature?

A
  • lesser curvature –> L and R gastric arteries (L gastric comes off the Celiac trunk; the two gastrics anastamose)
  • Greater curvature: L and R gastro-omental arteries (also anastomose with each other)
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30
Q

3 Portosystemic shunts (alleviate portal hypertension)

A

1) Esophageal varices –> anastomosis at the esophagus
2) Caput medusae –> anastomosis at the umbilicus
3) Internal hemorrhoids –> anastomosis at the rectum

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31
Q

type of hemorrhoids and cancers seen above and below the pectinate line:

A
  • above pectinate line:
  • internal hemorrhoids (not painful)
  • adenocarcinoma
  • below pectinate line:
  • external hemorrhoids (painful)
  • squamous cell carcinoma (main risk factor for squamous cell carcinoma here = HPV 16,18,31)
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32
Q

Pathway of bile: from production to secretion into duodenum:

A

Bile made in liver –> R and L hepatic ducts –> Common hepatic duct –> some into common bile duct, some into cystic duct –> from cystic duct, stored in gallbladder, then released back into cystic duct when needed, into common bile duct –> common bile duct meets pancreatic duct at Ampulla of Vater –> bile released via Sphincter of Oddi into Ampulla of Vater in duodenum!

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33
Q

Lodging of a gallstone where may lead to obstruction of both bile and pancreatic ducts?

A

if gallstone is lodged in Ampulla of Vater

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34
Q

What sort of tumor may obstruct the common bile duct?

A

Tumors of head of pancreas –> can compress ampulla, like a gallstone, thus obstructing common bile duct

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35
Q

Lateral to Medial organization of the Femoral Region:

A

Lateral: “NAVeL” :Medial

  • Nerve
  • Artery
  • Vein
  • Lymphatics
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36
Q

Femoral triangle:

  • formed by?
  • contains?
A
  • formed by:
  • inguinal ligament
  • sartorius muscle
  • adductor longus muscle
  • contains:
  • femoral nerve, artery, vein (lateral–>medial)
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37
Q

What does the femoral sheath contain?

A

-Contains femoral vein, artery, and lymphatics, but NOT femoral nerve

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38
Q

Sliding vs Paraesophageal Hiatal Hernias:

A
  • Both are types of diaphragmatic hernias, which occur at the gastro-esophageal jxn; stomach herniates upward through the esophageal hiatus of the diaphragm.
  • sliding hiatal hernia: GE jxn is displaced; have an “hourglass stomach”
  • paraesophageal hernia: GE jxn is normal; cardia of stomach moves into the thorax
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39
Q

“hourglass stomach”

A

sliding hiatal hernia

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40
Q

What kind of inguinal hernia occurs in infants?

A

INdirect inguinal hernia in INfants
–>goes through the INternal/deep inguinal ring, external/superficial inguinal ring, and into the scrotum (Basically, follows the path of the testes)

–>occurs in infants d/t failure of processus vaginalis to close

–> Covered by all 3 layers of spermatic fascia

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41
Q

What type of inguinal hernia passes through the inguinal/Hesselbach’s triangle?

A

Direct inguinal hernia

  • -> only covered by external spermatic fascia (unlike indirect, which is covered by all 3 layers)
  • ->usually in older men
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42
Q

Hernia that’s most common in women?

A

Femoral hernia

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43
Q

Hernia that’s a leading cause of bowel incarceration/obstruction?

A

Femoral Hernia

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44
Q

Hesselbach’s triangle:

  • borders?
  • what type of hernia goes through it?
A
  • Borders:
  • inguinal ligament
  • inferior epigastric artery
  • lateral border of rectus abdominis

*Direct inguinal hernias (older men) go through Hesselbach’s triangle

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45
Q

G cells (antrum of stomach) secrete?

A

Gastrin (“pro-gastric”)

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46
Q

I cells (duodenum, jejunum) secrete?

A

CCK (“pro-duodenum”, “anti-gastric”–> CCK stimulates pancreatic secretions)

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47
Q

S cells (duodenum) secrete?

A

Secretin (“pro-HCO3”, “nature’s antacid”)

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48
Q

D cells (pancreatic islets, GI mucosa) secrete?

A

Somatostatin (inhibits everything!)

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49
Q

Which hormone is increased in Zollinger-Ellison syndrome?

A

Gastrin

=”gastrinoma”

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50
Q

Which GI hormone is stimulated by Phenylalanine and Tryptophan?

A

Gastrin

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51
Q

What AAs may stimulate gastrin release?

A

Phenylalanine and Tryptophan

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52
Q

What does CCK cause?

A

Stimulates pancreatic secretion, gallbladder contraction, and gastric emptying

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53
Q

What does Secretin do?

A

Stimulates pancreatic HCO3- secretion, decreased gastric acid secretion, increased bile secretion
–> it’s “nature’s antacid” –> neutralizes gastric acid in duodenum to allow pancreatic enzymes to function

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54
Q

Somatostatin:

  • where is it secreted from?
  • what does it do?
A
  • secreted from D cells in pancreas (islets) and GI mucosa
  • inhibits:
  • ->decreased gastric acid and pepsinogen secretion
  • ->decreased pancreatic and intestinal secretions
  • ->decreased gallbladder contraction (so, if lots of somatostatin, may get biliary stones)
  • ->decreases insulin and glucagon release

***so overall inhibits digestion and absorption of substances needed for growth…

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55
Q

What is used more rapidly: oral glucose load or equivalent given by IV?

A

oral glucose is used more rapidly, d/t GIP = Gastric Inhibitory Peptide = Glucose-dependent insulinotropic peptide

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56
Q

VIP = Vasoactive Intestinal Peptide:

  • secreted from?
  • actions?
A

*source: Parasympathetic ganglia in sphincters, gallbladder, small intestine

  • actions:
  • increases intestinal water and electrolytes secretion
  • increases relaxation of intestinal smooth muscle and sphincters
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57
Q

VIPoma:

  • origin
  • symptoms?
A

non-alpha, non-beta pancreatic islet cell tumor

  • may be associated with MEN I
  • secretes VIP
  • symptoms:
  • ->tons of watery diarrhea (b/c VIP stimulates intestinal water and electrolyte secretion) –> so, as a result also have: dehydration, hypokalemia, etc…
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58
Q

Endocrine tumor that leads to lots of watery diarrhea?

A

VIPoma (pancreatic tumor, secretes tons of VIP)

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59
Q

Action = binds vitamin B12 to allow uptake of B12 in terminal ileum?

A

Intrinsic Factor

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60
Q

Which substances are secreted by Parietal Cells of stomach?

A
  • Intrinsic Factor

- Gastric Acid

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61
Q

Gastrinoma

A

gastrin-secreting tumor; get constant high levels of acid secretions and ulcers
–>=zollinger-ellison syndrome

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62
Q

Secreted by chief cells of stomach

A

Pepsin

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63
Q

Action of pepsin?

A

protein digestion

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64
Q

what activates pepsinogen–>pepsin?

A

Acid (H+)

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65
Q

Which cells secrete HCO3-?

A
  • mucosal cells (in stomach, duodenum, salivary glands, pancreas)
  • Brunner’s glands (in submucosa of duodenum)
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66
Q

How do NSAIDs lead to acidic damage in stomach?

A
  • Prostaglandins generate mucus that covers that covers the gastric epithelium
  • ->NSAIDs–>decrease PGs–> decrease mucus –> decrease HCO3- –> increased susceptibility to acidic damage in stomach
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67
Q

Which glands secrete saliva? What stimulates saliva secretion (PSNS, SNS?)? When is saliva hypotonic/isotonic?

A
  • secreted from parotid, submandibular, sublingual glands
  • stimulated by Sympathetic AND Parasympathetic activity
  • Normally is hypotonic, but is more isotonic with higher flow rates, b/c less time for absorption
  • **Sympathetic stimulation–> thicker secretions
  • **Parasympathetic stimulation–> watery secretions
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68
Q

How does Gastrin stimulate acid secretion in stomach?

A

G cells in antrum of stomach are stimulated by vagus nerve (via GRP transmitter)–> release Gastrin into circulation –> Gastrin stimulates ECL (EnteroChromaffin-Like) cells to release Histamine –> Histamine induces Parietal cells to secrete HCl

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69
Q

Affects of atropine on GI secretions?

A

Atropine = anti-cholinergic

  • -> blocks vagal stimulation of parietal cells (use ACh as transmitter)
  • -> BUT, no effect on G cell stimulation by vagal cells, because G cells use a different transmitter, GRP (not ACh) –> so, Gastrin can still stimulate parietal cells to secrete Intrinsic Facor and (via enterochromaffin-like cells and histamine) to secrete HCl
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70
Q

How do prostaglandins protect the stomach?

A
  • decrease acid secretion (Gi–>decreased cAMP–>decreased proton pumping)
  • increase mucus and HCO3- production
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71
Q

3 factors that stimulate G-cells to make Gastrin?

A
  • Hypercalcemia
  • Phenylalanine
  • Tryptophan
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72
Q

What may cause hypertrophy of Brunner’s glands?

A

Peptic ulcer disease (b/c lots of acid to deal with)
–>Brunner’s glands are located in duodenal submucosa; function = secrete alkaline mucus to neutralize acid contents entering duodenum from stomach

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73
Q

Trypsinogen:

  • secreted by?
  • converted to trypsin by?
  • action?
A
  • secreted by pancreas
  • enterokinase/enteropeptidase converts trypsinogen–>trypsin
  • converts other proenzymes/zymogens and more trypsinogen to active form
  • trypsin (and other zymogens)–> involved in protein digestion
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74
Q

alpha-amylase

A

secreted by pancreas

  • digests starch
  • **also have amylase in saliva, which digests starch in saliva
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75
Q

Lipase

A

secreted by pancreas

-digests fat

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76
Q

salivary amylase vs pancreatic amylase:

A
  • both digest starch
  • salivary: hydrolyzes alpha-1,4-linkages to form disaccharides
  • pancreatic: hydrolyzes starch to oligosaccharides and disaccharides
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77
Q

D-Xylose absorption test

A

Test to distinguish GI mucosal damage from other causes of malabsorption
–>D-xylose is normally easily absorbed by intestines; if problem with intestinal absorption, get low levels of D-xylose in urine and blood

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78
Q

SGTL1 = Sodium-Glucose-Co-Transporter:

A

Na-dependent transporter; absorbs Glucose and Galactose in enterocytes

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79
Q

GLUT-5

A

absorbs Fructose (by facilitated diffusion) into enterocytes

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80
Q

GLUT-2

A

Transports all monosaccharides (Glucose, Galactose, Lactose) from intestines into blood

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81
Q

Where in GIT is Iron absorbed?

A

Duodenum

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82
Q

Where in GIT is folate absorbed?

A

Jejunum

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83
Q

Where in GIT is Vitamin B12 absorbed?

A

Terminal ileum, along with bile acids; requires intrinsic factor (from parietal cells)!

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84
Q

Peyer’s patches:

  • where?
  • function?
A
  • located in ileum
  • Peyer’s patches = lymphoid tissue in lamina propria and submucosa of small intestine
  • function:
  • ->contain M-cells that take up antigen
  • ->B-cells stimulated in germinal centers of Peyer’s patches differentiate into IgA-secreting plasma cells. IgA ultimately resides in lamina propria. IgA protects gut from pathogens!
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85
Q

Lymphoid tissue of the GIT?

A

Peyer’s patches

  • located in ileum
  • B-cells in germinal centers of Peyer’s patches differentiate into IgA-secreting plasma cells –> IgA lives in lamina propria and protects gut from pathogens!
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86
Q

specialized M-cells that take up antigen in GIT?

A

-in Peyer’s patches –> the lymphoid tissue of GIT!

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87
Q

IgA in GIT comes from?

A

Peyer’s patches: have B-cells in germinal centers of Peyer’s patches (lymphoid tissue) that differentiate into IgA-secreting plasma cells
–>IgA protects the gut from pathogens!

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88
Q

Only way body can excrete cholesterol?

A

Bile

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89
Q

How is copper excreted from the body?

A

Bile; can’t excrete it in Wilson’s disease though…

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90
Q

3 functions of Bile:

A

1) Digest and absorb lipids and fat-soluble vitamins
2) Excrete cholesterol
3) Anti-microbial activity (by disrupting membranes)

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91
Q

Pale/Clay-colored stools?

A

-problem processing bilirubin

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92
Q

Cholestyramine

A
  • Bile Acid Resin –> a lipid-lowering agent
  • ->interferes with ability to reabsorb Urobilinogen–> so, more is excreted in stool or kidney; the liver then must use cholesterol to make more…
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93
Q

Colestipol

A

Bile-acid resin (like Cholestyramine; lipid-lowering agent)

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94
Q

Colesevelam

A

-Bile-acid resin (like cholestyramine; lipid-lowering agent)

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95
Q

Urobilin

A

breakdown product of bilirubin, excreted in urine; gives urine it’s color

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96
Q

Stercobilin

A

breakdown product of bilirubin, excreted in feces; gives color of stool (without it, have pale/clay-colored stool)

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97
Q

Urobilinogen

A
  • breakdown product of conjugated/direct bilirubin, after gut bacteria alter it in the gut; has 3 possible fates:
    1) excreted in feces as Stercobilin (about 80% of it)
    2) excreted in urine as Urobilin (very little of it –> about 2%)
    3) reabsorbed by liver via enterohepatic circulation (about 18% of it)
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98
Q

Biggest risk factor for a malignant salivary gland tumor?

A

Smoking

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99
Q

most common location of benign salivary gland tumor?

A

Parotid gland

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100
Q

Pleomorphic salivary gland adenoma:

A
  • most common salivary gland tumor

- painless, movable mass, benign, recurs

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101
Q

Warthin’s tumor

A

-benign salivary gland tumor; trapped in a lymph node, surrounded by lymph tissue

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102
Q

Mucooepidermoid carcinoma

A

-most common malignant salivary gland tumor

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103
Q

loss of Myenteric/Auerbach’s plexus?

A

Achalasia

  • ->can’t relax Lower Esophageal Sphincter
  • ->get esophageal aperistalsis
  • ->progressive dysphagia of solids and liquids (vs obstruction, which is dysphagia to solids only)
  • ->increased risk of esophageal carcinoma
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104
Q

Bird’s beak on barium swallow

A

Achalasia (esophageal aperistalsis; can’t relax LES d/t loss of Myenteric/Auerbach’s plexus)

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105
Q

2 conditions that may lead to secondary achalasia?

A
  • Chaga’s disease (mega-esophagus)

- CREST scleroderma (Esophageal dysmotility)

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106
Q

increased risk of what cancer with Achalasia?

A

–> esophageal carcinoma

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107
Q

progressive dysphagia of solids AND liquids, vs just solids vs progressive dysphagia first of solids THEN of liquids?

A
  • solids + liquids–> Achalasia
  • only solids–> obstruction
  • solids, then liquids–> esophageal cancer
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108
Q

Painless bleeding in lower 1/3rd of esophagus?

A

Esophageal varices

–>associated with portal HTN

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109
Q

Dysphagia + Glossitis (swollen, smooth tongue) + Iron-deficiency anemia

A

Plummer-Vinson syndrome

  • ->Dysphagia is d/t esophageal webs = thin membrane-like protrusion into esophagus
  • ->associated with increased risk of Squamous Cell Carcinoma of Esophagus
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110
Q

Boerhaave syndrome:

A
  • TRANSMURAL esophageal rupture d/t violent vomiting

- -> vs Mallory-Weiss which is just lacerations at the G-E jxn

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111
Q

Esophageal pathology associated with lye ingestion and acid reflux?

A

Esophageal strictures

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112
Q

Barrett’s esophagus: what sort of metaplasia occurs? increased risk of what kind of cancer?

A

Glandular metaplasia: squamous epithelium of distal esophagus is replaced with columnar/intestinal epithelium

  • d/t chronic GERD
  • assoc w/increased risk of Adenocarcinoma of esophagus
  • also associated with esophagitis and esophageal ulcers
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113
Q

What type of esophageal cancer is most common worlwide? in US?

A
  • worlwide: Squamous cell > Adenocarcinoma

- US: Adenocarcinoma > Squamous Cell

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114
Q
  • What part of esophagus is affected in each of these cancers?
  • What risk factors cause Squamous Cell Carcinoma?
  • What risk factors associated with Adenocarcinoma?
A
  • Squamous Cell: upper 2/3
  • smoking
  • alcohol
  • achalasia
  • esophageal webs (ie Plummer-Vinson syndrome)
  • Adenocarcinoma: lower 1/3
  • Barret’s esophagus
  • Esophagitis
  • Diverticula (like Zenker’s)
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115
Q

Whipple’s disease:

A
  • Tropheryma whippelii infection (gram +)
  • PAS + foamy macrophages in intestinal lamina propria
  • mostly older men
  • CAN:
  • ->cardiac symptoms
  • ->Arthralgias
  • ->Neurologic symptoms
  • **Also, classic malabsorption symptoms: diarrhea, steatorrhea, weight loss, weakness
  • treat with antibiotics!
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116
Q

Which part of intestine is affected in Celiac sprue?

A

-Proximal small bowel, mostly

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117
Q

What part of intestine is affected in lactase deficiency?

A

only tips of intestinal villi (b/c that’s where lactase is located)
–>so, get normal look villi

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118
Q

fat accumulation in enterocytes + malabsorption in childhood + neurologic manifestations?

A

Abeta-lipoproteinemia

  • ->have decreased synthesis of apo-B –> can’t generate chylomicrons –> decreased secretion of cholesterol and VLDL into bloodstream –> so, fat accumulates in enterocytes
  • **this is a malabsorption syndrome
  • treat with vitamin E supplementation (helps body produce some apoproteins)
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119
Q

Causes of pancreatic insufficiency? What must be supplemented?

A

Causes:

  • cystic fibrosis
  • obstructing cancer
  • chronic pancreatitis
  • get malabsorption of fat and fat-soluble vitamins (A, D, E, K)
  • get increased fat in stool
  • treat by pancreatic enzyme replacement, limit fat intake, and supplement A, D, E, K.
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120
Q

List the Malabsorption syndromes:

A

“These Will Cause Devastating Absorption Problems”

  • Tropical sprue
  • Whipple’s disease
  • Celiac sprue
  • Disaccharidase deficiency (like lactose intolerance)
  • Abetalipoproteinemia
  • Pancreatic insufficiency
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121
Q

Blunting of villi + Crypt hyperplasia in small intestines?

A

Celiac sprue

122
Q

Curling’s ulcer

A

Burning of the esophagus –> can lead to sloughing of gasric mucosa and Acute Erosive Gastritis

123
Q

Cushing’s ulcer

A

Brain injury that can lead to Acute Erosive Gastritis:

brain injury–> increased vagal stimulation –> increased ACh –> increased H+ production –> Gastritis

124
Q

Main causes of Acute Erosive Gastritis:

A

*Acute Erosive Gastritis = disrupton of mucosal barrier –> inflammation

  • Main causes:
  • Alcoholics
  • Pts taking daily NSAIDs (ie Rheumatoid Arthritis pts)
  • Curling’s ulcer = burning esophagus
  • Cushing’s ulcer = brain injury resulting in increased vagal stimulation
  • Stress
125
Q

Autoimmune disorder with:

  • autoantibodies to parietal cells
  • pernicious anemia (b/c no parietal cells, so no IF, so no B12)
  • Achlorydia (b/c no acid from parietal cells)
A

Chronic/Non-erosive gastritis of the Fundus/Body = Type A

126
Q

Cause of chronic/non-erosive gastritis to the fundus/body of the stomach

A

Autoimmune disorder with:

  • autoantibodies to parietal cells
  • pernicious anemia
  • achlorydia
127
Q

Cause of chronic/non-erosive gastritis affecting the antrum of the stomach?

A

H. pylori

  • this is the most common type of chronic gastritis
  • increased risk of MALT lymphoma
128
Q

What part of the stomach does H. pylori affect?

A

Antrum

129
Q

Disease in which rugae of stomach look like brain gyrae?

A

Menetrier’s disease

  • ->gastric hypertrophy
  • protein loss
  • parietal cell atrophy
  • increased mucous cells
  • precancerous
  • ->rugae are so hypertrophied that look like brain gyri!
130
Q

Main type of stomach cancer?

A

Adenocarcinoma (almost always)

131
Q

Acanthosis nigricans

A

seen in hyperinsulinemia and in visceral malignancies; often seen in gastric adenocarcinoma

132
Q

Virchow’s node:

A

metastasis from stomach to left supraclavicular node

133
Q

Krukenberg’s tumor:

A

bilateral metastasis from stomach to ovaries

–>see lots of mucus and signet ring cells in ovaries

134
Q

Sister Mary Joseph’s nodule:

A

metastasis from stomach adenocarcinoma to subcutaneous periumbilical area

135
Q

signet ring cells

A

cells seen in diffuse stomach cancer

  • ->filled with mucin; nucleus is pushed to periphery
  • ->see in stomach; also see if metastasis from stomach to ovaries (Krukenber’s tumor)
136
Q

Linitis Plastica

A

Stomach adenocarcinoma; stomach looks like a leather bottle –> thickened and leathery

137
Q

Pain is increased with eating? decreased with eating?

A
  • Increased with eating –> gastric peptic ulcer

* Decreased with eating –> duodenal peptic ulcer (b/c have bicarb secretion, which soothes ulcer)

138
Q

Role of H. pylori in gastric and duodenal peptic ulcers?

A
  • gastric ulcers–> H. pylori in 70% of cases

* duodenal ulcers–> H. pylori in about 100% of cases

139
Q

Is there an increased risk of cancer with Peptic Ulcer disease?

A

Trick question:

  • If gastric ulcer –> increased risk of carcinoma
  • If duodenal ulcer –> NO increased risk of carcinoma
140
Q

Recurrent ulcers despite treatment?

A

Check gastrin levels; may be Zollinger-Ellison syndrome

141
Q

Part of Intestines affected in Crohn’s?

A

Any part of GIT can be affected; but, usually involves terminal ileum and colon; have skip lesions
–>rectal sparing!

142
Q

Part of intestines affected in ulcerative colitis?

A
  • always the rectum

- then, have continuous colonic lesions up from there

143
Q

How much of intestinal wall is affected in Crohn’s? in Ulcerative colitis?

A

Crohn’s–> transmural

Ulcerative Colitis–> only mucosal and submucosal

144
Q

Creeping fat

A

Crohn’s

145
Q

Cobblestone mucosa

A

Crohn’s

146
Q

“string sign” on barium swallow

A

Crohn’s

147
Q

“lead pipe” appearance of intestines on imaging?

A

Ulcerative Colitis (d/t loss of haustra)

148
Q

IBD with: Noncaseating granulomas and Th1 mediated lymphoid aggegates on microscopy:

A

Crohn’s disease

no granulomas in UC; also UC is Th2-mediated

149
Q

IBD that has a higher association with colorectal cancer?

A

Ulcerative Colitis

Crohn’s also is associated with it; but higher risk with UC

150
Q

Treatment for Crohn’s?

A
  • Corticosteroids

- Infliximab

151
Q

Treatment for Ulcerative Colitis?

A
  • Aminosalicylic Acid preparations (like Sulfasalazine)
  • 6-MP
  • Infliximab
  • Colectomy
152
Q

STD that is commonly mistaken for IBD?

A

L1,L2, L3 subtypes of Chlamydia –> cause Lymphogranuloma venereum

153
Q

Dx criteria for IBS?

A

Recurrent abdominal pain + at least 2 of:

  • pain improves with defecation
  • change in stool frequency
  • change in appearance of stool
154
Q

McBurney’s point:

A

1/3 distance from ASIS to umbilicus (or 2/3 distance from umbilicus to ASIS!)
–>pain is localized here in appendicitis

155
Q

Risk/Complication of appendicitis?

A

Perforation–> get peritonitis

156
Q

“true” vs “false” diverticulum?

A

true: all 3 gut wall layers involved (ie Meckel’s)
false: only mucosa and submucosa outpouch

157
Q

Most common site of diverticula?

A

Sigmoid colon

158
Q

Most common cause of severe left lower quadrant pain?

A

Diverticulitis (inflammation of diverticula)

159
Q

Treatment for diverticulitis?

A

Antibiotics

160
Q

left lower quadrant pain + bright red rectal bleeding?

A

Diverticulitis

161
Q

stinky breath (halitosis) + dysphagia + esophageal obstruction?

A

Zenker’s diverticulum = “false” diverticulum at junction of pharynx and esophagus
–>have stinky breath d/t trapped food!

162
Q

Cause of Meckel’s diverticulum?

A

Persistent vitelline duct or yolk sac

163
Q

Most common congenital anomaly of GI tract?

A

Meckel’s diverticulum

164
Q

Pertechnetate study

A

Dx for Meckel’s diverticulum

165
Q

The five 2’s of Meckel’s diverticulum?

A
  • 2 inches long
  • 2 ft from ileocecal valve
  • 2% of popl
  • usually presents during first 2 years of life
  • may have 2 types of epithelia (gastric/pancreatic)
166
Q

currant jelly stools?

A

Intussusception

167
Q

Where does intussusception commonly occur?

A

commonly at ileocecal junction

168
Q

What age group does volvolus usually affect? Where does volvulus usually occur?

A
  • usually in elderly

- may occur at cecum and sigmoid colon (b/c have redundant mesentery)

169
Q

Congenital megacolon d/t failure of neural crest migration?

A

Hirschsprung’s disease

-lack of ganglion cells/enteric nervous plexuses (Auerbach’s and Messner’s) in segment of intestines

170
Q

What part of GIT is usually affected in Hirschsprung’s?

A

Involves rectum

171
Q

Failure to pass meconium?

A
  • Hirschsprung’s

- Cystic Fibrosis

172
Q

Increased risk of Hirschsprung in people with what other syndrome?

A

Down syndrome

173
Q

4 GI conditions associated with Down syndrome:

A
  • Hirschsprung
  • Celiac
  • Duodenal atresia
  • Annular pancreas
174
Q

Bilous vomiting in baby + “double bubble” (proximal stomach distention)

A

Duodenal atresia = blind duodenum

–>associated with Down syndrome

175
Q

Necrotizing enterocolitis: most common in what pt popl?

A

-preemie infants (b/c decreased immunity)

176
Q

Pain after eating in elderly + weight loss (but, not a gastric ulcer…)

A

ischemic colitis

–>usually occurs at splenic flexure (watershed area) and distal colon

177
Q

Sawtooth appearance of masses in gut lumen?

A

Colonic polyps

178
Q

Area often involved in colonic polyps?

A

-Rectosigmoid

179
Q

90% of colonic polyps are not malignant; which types are most likely to be malignant?

A

-Adenomatous, villous polyps (more villous the polyp, more likely to be malignant)

180
Q

multiple non-malignant hamartomas throughout GIT + hyperpigmented mouth, lips, hands, genitalia (so, hyperpigmented mucosal surfaces) + increased risk of Colorectal cancer?

A

Peutz-Jeghers syndrome

–>autosomal dominant

181
Q

autosomal dominant mutation of APC gene on chromosome 5q?

A

FAP = Familial Adenomatous Polyposis

–>100% of pts progress to colorectal cancer

182
Q

Lynch syndrome/HNPCC (Hereditary NonPolyposis Colorectal Cancer)

A
  • ->autosomal dominant mutation of DNA mismatch repair genes
  • -> 80% of pts progress to Colorectal Cancer
  • -> always involves proximal colon
183
Q

FAP + osseous and soft tissue tumors + retinal hypertrophy?

A

Gardner’s syndrome

184
Q

FAP + malignant CNS tumor?

A

Turcot’s syndrome

185
Q

“apple core” lesion on barium enema?

A

colorectal cancer

186
Q

CEA tumor marker

A

colorectal cancer

187
Q

Iron deficiency anemia in older males or post-menopausal females?

A

Suspect colorectal cancer

188
Q

Most common sites of carcinoid tumors?

A
  • appendix
  • rectum
  • ileum
189
Q

Bronchospasm + Flushing + Diarrhea + Right-sided heart lesion

A

Serotonin Syndrome (carcinoid tumor that secretes serotonin)

190
Q

Why is carcinoid syndrome only a “syndrome” once it metastasizes out of GI system?

A
  • -> b/c just tumor alone = carcinoid tumor, not syndrome
  • -> if tumor is in the GI, it may secrete serotonin, but don’t see any of the symptoms, b/c the liver metabolizes serotonin
  • ->once it metastasizes, usually to liver, then start seen symptoms associated with serotonin secretion; then it becomes “syndrome”
191
Q

form of bilirubin in bloodstream?

A

unconjugated bilirubin-albumin complex = indirect (water-insoluble) bilirubin

192
Q

form of bilirubin in liver?

A

conjugated/direct (water-soluble) bilirubin

193
Q

form of bilirubin in stool?

A

stercobilin

194
Q

form of bilirubin in urine?

A

urobilin

195
Q

uridine glucuronyl transferase = UDP glucuronyl transferase

A

enzyme, converts indirect bilirubin to direct bilirubin in liver

196
Q

Effects of Portal Hypertension

A
  • Esophageal varices –> Hematemesis
  • Melena
  • Splenomegaly
  • Caput medusae, ascites
  • Hemorrhoids
  • Portal hypertensive gastropathy
197
Q

Effects of liver cell failure:

A
  • Coma–> hepatic encephalopathy; from release of ammonia and other toxic metabolites from liver
  • Scleral icterus
  • musty smelling breath
  • gynecomastia
  • jaundice
  • testicular atrophy
  • asterixis (hand flap)
  • bleeding tendency (from decreased prothrombin and clotting factors)
  • anemia
  • ankle edema
198
Q

liver enzymes (AST, ALT) in alcoholic vs viral hepatitis?

A

alcoholic hepatitis: AST>ALT

viral hepatitis: ALT>AST

199
Q

Lactulose

A
  • Osmotic laxative
  • Also: Treatment for hepatic encephalopathy (in liver failure) –> b/c gut bacteria break it down, promoting nitrogen excretion as NH4+
200
Q

GGT (gamma-glutamyl transpeptidase)

A

serum marker for liver disease; elevated with heavy alcohol consumption

201
Q

decreased ceruloplasmin?

A

Wilson’s disease

202
Q

elevated amylase?

A
  • acute pancreatitis

- also elevated in MUMPS!

203
Q

elevated lipase?

A

acute pancreatitis

204
Q

elevated Alkaline Phosphatase?

A
  • non-specific:
  • obstructive liver disease (hepatocellular carcinoma)
  • bone disease
  • bile duct disease

*if elevated ALP, can then check GGT. If elevated GGT, then know it’s d/t liver disease

205
Q

What is Reye’s syndrome? What are the signs/symptoms?

A

=Childhood Hepatoencephalopathy:

  • ->mitochondrial abnormalities
  • ->fatty liver (microvesicular fatty change)
  • ->hypoglycemia
  • ->vomiting
  • ->hepatomegaly
  • ->coma

Mechanism: aspirin metabolites decrease Beta-oxidation by reversible inhibition of mitochondrial enzymes

206
Q

One disease when children should be treated with aspirin?

A

Kawasaki’s (to prevent coronary artery thrombosis)

207
Q

Best indicators of Liver function and progrnosis?

A

Prothrombin time and Serum albumin (albumin is made in liver, as are clotting factors)
*hypoalbuminemia + elevated PT = POOR prognosis.

208
Q

3 stages of alcoholic liver injury:

-Reversible?

A

1) Hepatic steatosis
- -> Macrovesicular steatosis/fatty change associated with moderate alcohol intake
- ->REVERSIBLE with alcohol cessation

2) Alcoholic hepatitis:
- ->from sustained, long-term alcohol intake
- ->swollen and necrotic hepatocytes; neutrophil infiltration
- ->Mallory bodies (intracytoplasmic eosinophilic inclusions)

3) Alcoholic cirrhosis:
- ->shrunken liver with “hobnail” appearance
- ->sclerosis around central vein
- ->looks like chronic liver disease: hypoalbuminemia, jaundice…
- ->IRREVERSIBLE

209
Q

Hepatic steatosis:

A
  • macrovesicular fatty change of liver; see hepatocytes filled with lipid droplets
  • Reversible effect of moderate alcohol intake; can reverse by stopping to drink alcohol
  • **can also get fatty liver from certain HIV drugs; metabolic syndrome; etc…
210
Q

Mallory bodies

A

intracytoplasmic eosinophilic inclusions within hepatocytes; see in alcoholic hepatitis

211
Q

7 diseases associated with increased risk of hepatocellular carcinoma:

A
  • Hepatitis B
  • Hepatitis C
  • Hemochromatosis
  • Carcinogens (specifically Alfatoxin from Aspergillus)
  • Alcoholic cirrhosis
  • alpha-1-antitrypsin deficiency
  • Wilson’s disease
212
Q

cancer associatd with elevated alpha-fetoprotein?

A

Hepatocellular carcinoma

213
Q

Common benign liver tumor in 30-50 year olds?

A
  • Cavernous Hemangioma

- ->DON’T biopsy it! b/c may lead to hemorrhage

214
Q

Nutmeg liver

A

Backup of blood into liver; d/t right heart failure and Budd-Chiari syndrome
–>if it persists, may result in cardiac cirrhosis

215
Q

Condition that looks similar to Right Heart Failure (Hepatomegaly, etc) BUT, absence of jugular venous distension:

A

Budd-Chiari syndrome

216
Q

Budd-Chiari syndrome:

A
  • Occlusion of IVC or hepatic veins –> leads to congestive liver disease (hepatomegaly, ascites, abdominal pain, eventually liver failure)
  • ->may have varices and visible abdominal/back veins
  • ->Looks kind of similar to Right heart failure, BUT absence of JVD
  • ->Associated with:
  • hepatocellular carcinoma
  • pregnancy
  • polycythemia vera
  • hypercoagulable state
217
Q

Liver cirrhosis + Panacinar Emphysema?

A

alpha-1-antitrypsin deficiency

–>this is a CODOMINANT trait

218
Q

PAS-positive globules in liver?

A

alpha-1-antitrypsin deficiency

219
Q

Cause of physiologic jaundice in neonates? Treatment?

A

Immature UDP-glucuronyl transferase at birth (physiologic): can’t convert unconjugated bilirubin to conjugated in liver –> get unconjugated/indirect hyperbilirubinemia –> Jaundice

*Treat with phototherapy: converts unconjugated bilirubin to a water-soluble form, so it can be renally excreted! COOL!

220
Q

What is jaundice? What are the 3 causes/types of pathologic jaundice (not counting physiologic neonatal jaundice)?

A

Jaundice = yellowing of skin and/or sclerae d/t elevated bilirubin

  • Causes:
  • Hepatocellular injury
  • Obstruction to bile flow
  • Hemolysis
221
Q

Jaundice, elevated bilirubin in response to fasting, stress, exercise?

A
  • -> Gilbert’s syndrome
  • -> have mildly decreased UDP-glucuronyl transferase (so decreased conversion of indirect to direct bilirubin) or decreased bilirubin intake
  • ->mild disease; quite common, but most pts don’t even know they have it
  • ->when flares: have indirect hyperbilirubinemia
222
Q

pathologic jaundice early in life + kernicterus (bilirubin deposition in brain) + elevated unconjugated bilirubin

A

Crigler-Najjar Syndrome Type 1
–>absent UDP-glucuronyl transferase (so can’t convert indirect to direct bilirubin) –> get elevated indirect/unconjugated bilirubin

223
Q

Treatment for Crigler-Najjar syndrome type 1?

A
  • phototherapy (makes Unconjugated bilirubin water-soluble, so can excrete in urine)
  • Plasmapheresis (get rid of excess unconjugated bilirubin)

–>Crigler Najjar type 1 is fatal within a few years

224
Q

Crigler-Najjar type 2:

  • what is it?
  • treatment?
A

milder form of Crigler-Najjar type 1; have decreased amount of UDP-glucuronyl transferase (not absent, as in type 1)
–>can treat with phenobarbital (increases synthesis of liver enzymes, including UDP glucuronyl transferase)

225
Q

Phenobarbital

A

Treatment for Crigler-Najjar type 2 (and can be used for symptomatic Gilbert’s)
–>increases synthesis of liver enzymes –> so, increases synthesis of UDP-glucuronyl transferase

226
Q

Conjugated Hyperbilirubinemia + Black liver on gross examination
–>otherwise benign

A

=Dubin-Johnson syndrome

–>defective liver excretion of bilirubin; so get elevated conjugated bilirubin in blood

227
Q

Rotor’s syndrome:

A

mild disorder, similar to Dubin-Johnson syndrome (but less severe); have defective liver excretion of bilirubin, so mildly elevated conjugated bilirubin in blood; unlike Dubin-Johnson syndrome, does not cause black liver

228
Q

Disease d/t problem with bilirubin uptake into liver?

A
  • Gilbert’s

- ->elevated unconjugated bilirubinemia

229
Q

Diseases d/t problem with bilirubin conjugation

A
  • Gilbert’s
  • Crigler-Najjar types 1 and 2
  • physiologic neonatal jaundice

–>elevated unconjugated bilirubinemia

230
Q

Diseases d/t problem with bilirubin excretion from liver?

A
  • Dubin-Johnson
  • Rotor’s

–>elevated direct/conjugated bilirubinemia

231
Q

Penicillamine

A

Treatment for Wilson’s disease

232
Q

Kayser-Fleischer ring

A

yellow-green-golden brown corneal ring seen in Wilson’s disease

233
Q

decreased levels of ceruloplasmin?

A

seen in Wilson’s disease

–>ceruloplasmin=major copper-carrying protein in blood

234
Q

Signs/symptoms of Wilson’s disease: “CCCCCopper is Hella BADDD”

A
  • decreased Ceruloplasmin
  • Corneal deposits = Kayser-Fleischer rings
  • Cirrhosis
  • Copper accumulation (in liver, brain, cornea, kidneys, joints, etc)
  • hepatocellular Carcinoma (increased risk)
  • Hemolytic anemia
  • Basal ganglia degeneration (specifically, degeneration of PUTAMEN); get parkinsonian symptoms
  • Asterixis
  • Dementia
  • Dyskinesia
  • Dysarthria

***Treat with Penicillamine

235
Q

What part of brain is degenerated in Wilson’s disease?

A

Basal ganglia, specifically Putamen, degeneration

–>get Parkinsonian symptoms

236
Q

micronodular Cirrhosis + Diabetes + skin pigmentation?

A

Hemochromatosis = “Bronze” diabetes

237
Q

Deferoxamine

A

Treatment for hereditary Hemochromatosis

–>also do repeated phlebotomy

238
Q

Causes of hemochromatosis?

A
  • herditary (autosomal recessive)

- secondary to repeated blood transfusions (ie in Beta-thalassemia major)

239
Q

lab findings in Hemochromatosis: ferritin, iron, TIBC, transferring?

A
  • elevated ferritin (stores iron within cells)
  • elevated iron
  • decreased TIBC (indirect measure of transferrin, which transports iron in blood)
  • elevated transferritin saturation (serum Fe/TIBC)
240
Q

Which HLA is associated with hemochromatosis?

A

HLA-A3

241
Q

Complications/Results of Hemochromatosis:

A
  • CHF
  • Testicular atrophy in males
  • increased risk of hepatocellular carcinoma
242
Q

Cause of primary biliary cirrhosis?

A
  • ->Autoimmune reaction: get lymphocytic infiltrate and granulomas
  • ->mostly seen in middle-aged women
  • ->anti-mitochondrial antibodies
243
Q

Elevated anti-mitochondrial antibodies?

A

Primary biliary cirrhosis

244
Q

Causes and pathophysiology of Secondary Biliary Cirrhosis?

A

–>Extrahepatic biliary obstruction (like a gallstone, biliary stricture, carcinoma of head of pancreas, chronic pancreatitis) –> so, get increased pressure in intrahepatic ducts –> injury and fibrosis –> bile stasis

245
Q

“onion skin” bile duct fibrosis?

A

Primary Sclerosing Cholangitis (a biliary tract disease)

246
Q

Presentation and Labs in Biliary Tract Diseases (Primary and Secondary Biliary Cirrhosis, Primary Sclerosing Cholangitis):

A

Presentation:

  • Pruritis
  • Jaundice
  • Dark urine (b/c elevated urobilinogen in urine)
  • Pale stools (b/c bile not making it into stools)
  • Hepatosplenomegaly

Labs:

  • Conjugated/Direct Hyperbilirubinemia
  • elevated cholesterol
  • elevated ALP
247
Q

Pruritus in a middle-aged woman + elevated conjugated bilirubinemia?

A
  • ->Consider primary biliary cirrhosis

- ->may also consider primary sclerosing cholangitis

248
Q

Complication of Secondary Biliary Cirrhosis?

A

Ascending cholangitis = infection of biliary tree (makes sense, b/c have an obstruction of bile flow; bile stasis; etc…)

249
Q

What condition is Primary Sclerosing Cholangitis associated with?

A

Ulcerative Cholitis

-primary sclerosing cholangitis can also lead to secondary biliary cirrhosis

250
Q

Biliary tract disease with Hypergammaglobulinemia (IgM)?

A

–>Primary sclerosing cholangitis

251
Q

5 main risk factors for gallstones/cholelithiasis:

A

5 F’s:

  • Female
  • Forty
  • Fat
  • Fertile (multiparity)
  • Feathers (Native Americans)
252
Q

Charcot’s triad of cholangitis (infection of biliary tree/common bile duct):

A

1) Jaundice
2) Fever
3) RUQ pain

253
Q

Murphy’s sign

A
  • ->positive in cholecystitis; good way to dx pain in the RUQ
  • ->positive: when deeply palpate, pt has inspiratory arrest b/c such deep pain
254
Q

Pain on deep palpation, causing inspiratory arrest

A

Positive Murphy’s sign

–> positive in cholecystitis; way to dx RUQ pain

255
Q

3 causes of gallstones:

A
  • elevated cholesterol and/or bilirubin
  • decreased bile salts
  • gallbladder stasis

–>all of these can cause stones

256
Q

Most common cause of cholecystitis (inflammation of gallbladder)?

A

Gallstones

–>have positive Murphy’s sign!

257
Q

Ascending cholangitis =

A

inflammation of bile duct; usually d/t obstruction of duct by gallstones

258
Q

What is acute pancreatitis?

A

=autoingestion of pancreas by pancreatic enzymes. ouch.

259
Q

Causes of Acute Pancreatitis:

A

“GET SMASHED”

  • ->Gallstones and Ethanol = Most common causese
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune disease
  • Scorpion sting
  • Hypercalcemia/Hypertriglyceridemia
  • ERCP (Endoscopic Retrograde Cholangiopancreatography = endoscopic technique to dx/treat problems of pancreatic or biliary ducts; but, main risk of it = acute pancreatitis)
  • Drugs (ie sultas, HIV drugs…)
260
Q 
#1 cause of chronic pancreatitis?
-other main cause?
A 
#1 = alcoholism
other main cause = smoking
261
Q

labs in acute pancreatitis:

A

-elevated amylase and lipase (lipase = more specific)

262
Q

steatorrhea, fat-soluble vitamin deficiency, diabetes

A

pancreatic insufficiency; may be a result of chronic pancreatitis (which is usually d/t alcoholism or smoking)

263
Q

CA-19-9

A

specific tumor marker for Pancreatic adenocarcinoma

264
Q

CEA

A

less specific tumor marker for pancreatic adenocarcinoma

265
Q

painless jaundice in male >50 years old?

A

consider Pancreatic adenocarcinoma

266
Q 
#1 risk factor for Pancreatic Adenocarcinoma?
-other risk factors?
A

1 = Smoking (but, not alcoholism)

  • other risk factors:
  • chronic pancreatitis (which is usually caused by alcoholism or smoking… kind of contradicts the not alcoholism thing…)
  • Jewish and African American males
  • > 50 years old
  • Diabetes
  • Genetics
267
Q

Courvoiseier’s sign:

A
  • obstructive jaundice with palpable gallbladder
  • ->pruritus, dark urine, pale stools (all signs of obstructive jaundice…)
  • ->see with pancreatic adenocarcinoma
268
Q

Trousseau’s syndrome:

A
  • migratory thrombophlebitis–> redness and tenderness on palpation of extremities
  • ->see with pancreatic adenocarcinoma
269
Q

Presentation of pancreatic adenocarcinoma:

A
  • abdominal pain that radiates to back
  • weight loss
  • redness and tenderness on palpation of extremities (migratory thromboephlebitis = Trousseau’s sign)
  • Obstructive jaundice and palpable gallbladder –> pruritus, dark urine, pale stools (=Courvoiseier’s sign)
270
Q

Asterixis:

A

See in:

  • liver cell failure
  • Wilson’s disease
  • Uremia (increased BUN and Creatinine, like in renal failure)
271
Q

Drugs that end in “-dine”

A

H2 blockers: Cimetadine, Ranitidine, Famotidine, Nizatidine

–> take H2 blockers before you “dine”

272
Q

Ranitidine

A

H2 blocker

273
Q

Cimetidine

A

H2 blocker

  • ->inhibits cytochrome P450!
  • ->also:
  • gynecomastia, impotence, decreased libido in males (anti-androgen effects)
  • can cross BBB (headaches, dizziness, confusion)
  • can cross placenta
274
Q

Famotidine

A

H2 blocker

275
Q

Nizatidine

A

H2 blocker

276
Q

Drugs that can cause gynecomastia? (random, not necessarily GI)

A

“Some Drugs Create Awesome Knockers”

  • Spirinolactone
  • Digitalis
  • Cimetidine
  • Alcohol
  • Ketoconazole
277
Q

Mechanism of H2 blockers?

A
  • reversibly block Histamine (released from ECL cells, after stimulation by Gastrin) from binding to the H2 receptor on gastric parietal cells
  • ->get decreased cAMP, meaning no stimulation of the ATP-ase –> decreased H+ secretion from parietal cells into gastric lumen
278
Q

What are more potent drugs: H2 blockers or PPIs?

A

PPIs are more potent than H2 blockers; so, use H2 blockers for less severe cases; PPIs for more severe

*note: H2 blockers are reversible; PPIs are irreversible

279
Q

drugs ending in “-prazole”

A

PPIs (proton pump inhibitors)

  • Omeprazole
  • Lansoprazole
  • Pantroprazole
  • Esomeprazole
280
Q

Omeprazole

A

PPI

281
Q

Lansoprazole

A

PPI

282
Q

1st line treatment for Zollinger-Ellison syndrome?

A

Proton Pump Inhibitors

283
Q

Mechanism of PPIs?

A

Irreversibly inhibit Proton Pump (H/K-ATPase) in parietal cells (so, can’t excrete H+ into gastric lumen from parietal cells)

284
Q

Bismuth

A
  • treatment of ulcers and traveler’s diarrhea
  • mechanism: binds to ulcer base, providing physical protection; thus allowing HCO3- secretion to reestablish pH gradient in mucus layer
285
Q

Sucralfate

A

Same mechanism as bismuth; treatment of ulcers and traveler’s diarrhea

  • ->bind to ulcers, providing physical protection; allows HCO3- secretion to reestablish pH gradient in mucus layer
  • Requires an acidic environment to polymerize; WONT WORK IF TAKING ANTACIDS CONCURRENTLY!
286
Q

Misoprostol:

  • mechanism
  • clinical uses
  • side effect
  • contraindications
A
  • Prostaglandin analog
  • Mechanism: binds receptor on parietal cell –> stimulates Gi –> decreased cAMP –> decreased stimulation of Proton Pump –> decreased acid production/secretion into gastric lumen
  • Clinical uses:
  • Prevent NSAID-induced peptic ulcers (b/c NSAIDs decrease prostaglandins)
  • Treatment of PDA
  • Induce labor
  • Side effect:
  • Diarrhea
  • Conraindication:
  • Pregnant women/women of child-bearing age (b/c induces labor)
287
Q

Octreotide:

  • mechanism
  • clinical uses
A

Somatostatin analog
*Somatostatin/Octreotide –> Gi –> blocks/decrease cAMP –> blocks Proton Pump –> decreased acid secretion into gastric lumen

  • Uses:
  • secretory diarrhea
  • acute variceal bleeds
  • acromegaly (inhibits GH)
  • VIPoma (pancreatic islet cell tumor that secretes lots of Vasoactive Intestinal Polypeptide, causing lots of diarrhea)
  • Carcinoid tumors
288
Q

Treatment of VIPoma?

A

Octreotide

289
Q

Treatment of Carcinoid Syndrome?

A

Octreotide

290
Q

Diphenoxylate

A

opiate-anti-diarrheal drug;

–>binds to Mu opiate receptors in GI tract and slows motility

291
Q

Side effects of Antacids?

A
  • all can cause hypokalemia (b/c block H/K-ATPase)

- Can chelate and decrease effectiveness of other drugs

292
Q

Side effects of Aluminum Hydroxide (antacid) overuse?

A
  • “aluMINIMUM of feces”= constipation
  • hypokalemia and decrease efficacy of other drugs (all antacids)
  • others
293
Q

Side effects of Magnesium Hydroxide (antacid) overuse:

A

“Must Go to the bathroom” = diarrhea

  • hypokalemia and decrease efficacy of other drugs (all antacids)
  • others
294
Q

Side effects of Calcium carbonate (antacid = TUMS!)

A
  • Hypercalcemia
  • may cause rebound increase in acid!
  • hypokalemia and decrease efficacy of other drugs (all antacids)
295
Q

Magnesium hydroxide

A
  • osmotic laxative

- also an antacid (with side effect of diarrhea!)

296
Q

Magnesium citrate

A

-osmotic laxative

297
Q

Polyethylene glycol

A

Osmotic laxative

298
Q

Infliximab clinical uses?

A
  • monoclonal anti-TNF antibody
  • Uses:
  • Crohn’s disease
  • Rheaumatoid arthritis
299
Q

Sulfasalazine:

  • mechanism?
  • clinical uses?
A

=combo of Sulfapyridine (antibacterial) + 5-ASA (aminosalicylic acid = anti-inflammatory)
–>activated by colonic bacteria (so, only effective in distal ileum and colon)

  • clinical uses:
  • Ulcerative Colitis (always)
  • Crohn’s (but, only acts in distal ileum and colon; so, only if disease is localized to those areas, which it often is)
300
Q

Odansetron:

  • mechanism
  • clinical uses
  • side effects
A

=anti-serotonin and anti-emetic

  • Clinical uses:
  • pts undergoing chemo, to combat nausea/vominiting
  • pregnant women with morning sickness
  • side effects:
  • headache (think opposite of triptans, which are serotonin-agonists; relieve headaches)
  • constipation (think opposite serotonin/carcinoid syndrome, which causes diarrhea)
301
Q

Metoclopramide:

  • mechanism
  • uses
  • toxicity/side-effects
  • contraindications
A

=D2-receptor antagonist (Dopamine-blocker)

  • uses:
  • diabetic and post-surgery gastroparesis (delayed gastric emptying)
  • Toxicities/Side effects:
  • may lower seizure threshold
  • parkinsonian symptoms (b/c block dopamine)
  • diarrhea, etc…
  • Contraindications:
  • Parkinson’s disease (duh)
  • small bowel obstruction (duh)
302
Q

4 Drugs that may lower seizure threshold? (random, not specific to GI)

A

1) Metoclopramide (treats gastroparesis)
2) Buproprion (anti-depressant w/out sexual side effects; increased seizures, especially pts with bulemia or anorexia)
3) Tramadol (used to treat chronic pain; weak opiod-agonist; inhibits serotonin and NE reuptake, but not used to treat depression)
4) Enflurane (inhaled anesthetic)

FirstAID (24 decks)

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