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1
Q

baby vomits milk when fed and has a gastric air bubble. What kind of fistula is present?

A

blind esophagus w/ lower segment of esophagus attached to trachea

2
Q

After a stressful life event, 30 y/o female has diarrhea and blood per rectum; intestinal bx shows transmural inflammation. what is thedx

A

crohn’s dz

3
Q

young man presents w/ mental deterioration and tremors. he has brown pigmentation in a ring around the periphery of his cornea and altered LFTs. What tx should he receive?

A

penicillamine for wilson’s dz

4
Q

20y/o male presents w/ idiopathic hyprbilirubinemia. what is the most common cause?

A

Gilberts dz

5
Q

Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
Foregut

A

Celiac aa

stomach to prox duodenum, liver, gallbladder, pancreas

6
Q

Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
midgut

A

SMA

distal duodenum to prox 2/3 of transverse colon

7
Q

Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
hndgut

A

IMA

distal 1/3 of transvere colon to upper portion of the rectum

8
Q

Stoach recieves main blood supply from branches of this ________

A

celiac trunk

9
Q

because of portal-systemic anastomoses blockage of 1 vv can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.

L gastric →azygous

What is this a common complication with?

A

esophageal varicies

Portal HTN

mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension

10
Q

because of portal-systemic anastomoses blockage of 1 aa can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.

Superior →inferior rectal

What is this a common complication with?

A

external hemorrhoids

mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension

11
Q

because of portal-systemic anastomoses blockage of 1 vv can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.

Paraumbilical →inferior epigastric

What is this a common complication with?

A

caput medusae at naval

mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension

12
Q

because of portal-systemic anastomoses blockage of 1 artery can result in congestion of blood in an alternate route. What two places do the the retroperitonal vv usually back up to?

A

renal and paravertebral vv

13
Q

layers of gut wall (inside to outside)[pic.p.264]

A

1) mucosa
2) submucosa
3) muscularis externa
4) serosa/adventita

14
Q

mucosal layer consists of these three layers (give fxs as well)

A
epithelium (absorption)
lamina propria (support)
muscularis mucosa (mucosal motility
15
Q

Submucosa includes this nerve plexus that controls these fxs

A

Submucosal (Meissner’s)

controls Secretions, blood flow, and absorption

16
Q

Muscularis externa includes this nerve plexus that controls these fxs

A

Myenteric nerve plexis (Auerbach’s)

controls mobility

17
Q

Muscularis externa has these two layers of mm

A

outer longitudinal layer

inner circular layer

18
Q

This enteric nerve plexus coordinates MOTILITY along the entire gut wall. It contains cell bbodies of some parasympathetic terminal effector neurons. It is located between inner and outer layers (longitudinal and circular) smooth mm in the GI tract wall

A

Myenteric (Auerbach’s) plexus

19
Q

This enteric nerve plexus regulates local SECRETIONS, blood flow, and absorption. It contains cell bodies of some parasympathetc terminal effector neurons. It is located between the mucosal and inner layer of smooth mm in the GI tract wall.

A

Submucosal (Meissner’s) plexus

20
Q

These glands secrete alkaline mucus to neutrolize acid contents entering the duodenum from the stomach. They are located in the duodenal submucosa.

A

brunners glands

21
Q

these are the only GI submucosal glands

A

brunner’s glands

22
Q

hypertrophy of Brunner’s glands is seen in what dz

A

Peptic Ulcer dz

23
Q

Unencapsulated lymphoid tissue found in lamina propria and submucosa of the small intestine

A

Peyer’s patch

24
Q

Peyer’s patches are covered by a single layer of cuboidal enterocytes with specialized _____ cells intersperced.

A

M cells

25
Q

Are their goblet cells in peyer’s patches

A

no

26
Q

______ take up antigen.

A

M cells.

27
Q

Stimulated _____ leave Peyer’s patch and travel through lyph and blood to lamina propria of the intestine, where they differentiate into __________.

A

M cells

IgA-secreting plasma cells

28
Q

_____ receives protective secretory component and is then transported across epithelium to gut to deal with intraluminal Ag

A

IgA

29
Q

Irregular “capillaries” with fenestrated endothelium (pores 100-200 nm in diameter). No basement membrane. Allows macromolecules of plasma full access to basal surface of hepatocytes through perisinusoidal space (space of Disse)

A

Sinusoids of liver

30
Q

line formed where hindgut meets ectoderm

A

pectinate line

31
Q

Above pectinate line or below pectinate line:

internal hemorrhoids (not painful)

A

above pectinate line

32
Q

Above pectinate line or below pectinate line:

external hemorrhoids (painful)

A

below pectinate line

33
Q

Above pectinate line gets _________ innervation (visceral or somatic innervation)

A

Viscral

34
Q

internal hemorrhoids receive ________ innervation

A

visceral

35
Q

arterial supply of above the pectinate line is from the _________

A

superior rectal artery (branch of IMA)

36
Q

venous drainage of above the pectinate line is to the _________ to the IMV to the portal system

A

supierior rectal vein

37
Q

cancer associated with above pectinate line is _________

A

adenocarcinoma

38
Q

Below pectinate line is innervated via ________ innervation

A

somatic

39
Q

external hemorrhoids recieve _______ innervation and are therefore quite painful

A

somatic

40
Q

cancer associated with below pectinate line

A

squamous cell carcinoma

41
Q

arterial supply to below pectinate line

A

inferior rectal aa (branch of internal pudendal aa)

42
Q

venous drainage of below pectinate line is to _______ to internal pudendal vv to internal iliac vv to IVC

A

inferior rectal vv

43
Q

lateral to medial in the femoral triangle

which of these sxs lie inside the femoral sheath

A

femoral nn, aa, vv, empty space and lymphatics (deep inguinal LNs

all except femoral nn lie in the sheath

mneu: N-(AVEL)

44
Q

what sxs make up the femoral triangle

A

1) sartorius mm
2) inguinal ligament
3) adductor longus mm

45
Q

this drug class consists of Cimetidine, rantidine, famotidine, nizatidine

A

H2 blockers

46
Q

these drugs reversibly block histamine H2 receptors leading to decreased H+ secretion by parietal cells

A

H2 blockers (tidines)

47
Q

these drugs are used for peptic ulcer, gastritis, mild esophageal reflux

A

H2 blockers (tidines)

48
Q

This drug is a potent inhibitor of P-450; it also has an antiadrogenic effect and decreased renal excretion of cratinine. Other H2 blockers are relatively free fo these effects

A

Cimetidine

49
Q

these drugs include omeprazole, lansoprazole

A

protone pump inhibitors (prazoles)

50
Q

these drugs work by irreversibly inhibiting H+/K+ATPase in stomach parietal cells

A

protone pump inhibitors (prazoles)

51
Q

These drugs are used for peptic ulcers, gastritis, esophageal reflux, and zollinger-ellison syndrome

A

protone pump inhibitors (prazoles)

52
Q

these drugs work by binding to the ulcer base, providing physical protection, and allowing HCO3- secretion to reestablish pH gradient to the mucus layer

A

Bismuth, sucralfate

53
Q

these drugs are used to help in ulcer healing and traveler’s diarrhea

A

Bismuth, sucralfate

54
Q

triple therapy of H. pylori ucers includes

A

1) metronidazole
2) bismuth
3) amoxicillin (or tetracycline)

55
Q

this drug is a PGE1 analog that increases production and secretion of gastric mucous barrier, and decreases acid production

A

misoprostol

56
Q

this drug is used clinically to prevent NSAID-induced peptic ulcers, maintain a patent ductus arteriosus, and to induce labor

A

misoprostol

57
Q

toxicity of this drug includes diarrhea. It is contraindicated in women of childbearing potential (abortifacient)

A

misoprostol

58
Q

drugs of these this class includes pirenzepine & propantheline

A

muscarinic antagonist

59
Q

these drugs act by blocking M1 receptors on Enterochromaffin-like (ECL) cells (decreasing histamine secretion) and M3 receptors on parietal cells (decreased H+ secertion)

A

Muscarinic antagoinists

60
Q

these drugs are clinically indicated only for peptic ulcer

A

muscarinic antagonist

61
Q

these drugs toxicieite include bradycardia, dry mouth, difficulty focusing eyes

A

muscarinic antagonist

62
Q

this drug is a monoclonal antibody to TNF-alpha, a proinflammatory cytokine

A

infliximab

63
Q

this drug is used for Crohn’s dz & rheumatoid arthritis

A

infliximab

64
Q

this drug for crohns dz and arthritis has toxicities that include respiratory infection, fever, hypotension

A

infliximab

65
Q

These drugs act with a combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory) which is activated by colonic bacteria.

A

sulfasalazine

66
Q

this drug is used clinically for ulcerative colitis & crohn’s dz

A

sulfasalazine

67
Q

the toxicities of this drug include malaise, nausea, sulfonamide toxicity, reversible oligospermia

A

sulfasalazine

68
Q

This drug is a 5-HT3 antagonist.

A

Ondansetron

69
Q

this drug is used to control vomiting postoperatively and in patients undergoing cancer chemotherapy

A

ondansetron

you will not vomit with ONDANSetron, so you can go ON DANCing.

70
Q

toxicities of this antiemetic include headache and constipation

A

ondansetron

71
Q

overuse of these drugs can affect absorption, bioavaiability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying

A

antacid

72
Q

Antacids:

Primary SEs of Aluminum hydroxide

A

constipation and hypophosphetemia

mneu: aluMINIMUM amount of feces

73
Q

Antacids:

Primary SEs of magnesium hydroxide

A

diarrhea

mneu: Mg- Must Go to the bathroom

74
Q

Antacids:

Primary SEs of calcium carbonate

A

hypercalcemia and rebound acid increase

75
Q

all antacids can cause _______

A

hypokalemia

76
Q

This is a very aggressive CA, prognosis averages 6 mo. or less, usually already metastasized at presentation.

A

panceratic adenocarcinoma

77
Q

pancreatic adenocarcinomas are more common in the pancreatic ______(head or tail)

A

head–obstuctive jaundice

78
Q

this often presents with:

1) abd pain radiating to back
2) weight loss (due to malabsorption & anorexia)
3) migratory thrombophlebitis (trousseau’s syndrome)
4) obstructive jaundice w/ palpable gallbladder (courvoisier’s sign)

A

pancreatic adenocarcinoma

79
Q

this is caused by activation of pancreatic enzymes leading to autodigestion

A

acute pancreatitis

80
Q

causes of acute pancreatitis

A
Gallstones
Ethanol
Trauma
Steroids
Mumps
Auutoimmune dz
Scorpion sting
Hypercalcemia/Hyperlipidemai
Drugs (e.g., sufla drugs)

mneu: GET SMASHeD

81
Q

this can cause fatal pancreatitis

A

ddI (videx)

82
Q

what is the clinical presentaton of acute pancreatitis

A

pt presents w/ epigastric abdominal pain raiating to back with anerexia and nausia

83
Q

what 2 labs will be elevated in acute pancratitis

A

amylase, lipase

84
Q

amylase and lipase which has the higher specificity

A

lipase

85
Q

acute pancreatitis can lead to (give 3)

A

DIC, ARDS, diffuse fat necrosis, hypocalcemia, pseudocyst formation, hemorrhage, and infection

86
Q

chronic calcifying pancreatitis is strongly associated with _______

A

alcoholism

87
Q

chronic obstructive pancreatitis is stongly associated with ______

A

gallstones

88
Q

these form when solubizing bile acids and lecithin are overwhelmed by increased cholesterol and/or bilirubin

A

gallstones

89
Q

risk factors for gallstones

A

1) fat
2) female
3) fertile
4) forty

90
Q

3 types of gallstones

A

1) cholesterol stones
2) mixed stones
3) pigment stones

91
Q

these stones are radioluscent with 10-20% opacity due to calcifications. They are associated with obesity, Crohn’s dz, cystic fibrosis, advanced age, clofibrate, estrogens, multiparity, rapid weight loss, and Native American origin

A

Cholesterol stones

92
Q

these stones are the most common type. They are radioluscent and they have both cholesterol and pigment components.

A

mixed stones

93
Q

these stones are radiopaque. They are seen in pts w/ chronic RBC hemolysis, alcoholic cirrhosis, advanced age, and biliary infection.

A

pigment stones

94
Q

how do you dx gallstones

A

US

95
Q

how do you tx gallstones

A

cholecystectomy

96
Q

rare, often fatal childhood hepatoencephalopathy. Findings include fatty liver (microvesicular fatty change), hypoglycemia, and coma. It is associated with viral infection (especially VZV and infuenza B) and salysylates; thus, aspirin is no longer recommended for children (use acetaminophen, with caution)

A

Reye’s syndrome

97
Q

Most common primary malignant tumor of the liver in adults.

A

hepatocellular carcinoma (hepatoma)

98
Q

this CA is associated with hepatitis B & C, Wilson’s dz, hemochromatosis, alpha 1 antitripsin deficiency, alcoholic cirrhosis, and carcinogins (e.g., aflatoxin B1)

A

hepatocellular carcinoma.

99
Q

this CA can present with tender hepatomegaly, ascites, polycythemia, and hypoglycemia

A

hepatocellular carcinoma

100
Q

hepatocellular carcinoma, like renal cell carcinoma, is commonly spread via this method of dissemination

A

hematogenous

101
Q

HCC shows elevated serum _________ level

A

alpha fetaprotien

102
Q

HCC may lead to this syndrome ______.

A

Budd-Chiari syndrome

103
Q

intrahepatic, autoimmune disorder characterized by severe obstructive jaundice, statorrhea, pruritis, hypercholesterolemia (xanthoma).

labs show: ↑alk phos, ↑ serum mitochondrial Ab

A

primary billiary cirrhosis

104
Q

this disorder is due to extrahepatic biliary obstruction. Increased pressure in intrahepatic ducts leading to injury/fibrosis. Often complicated by ascending cholangitis (bacterial infection), bile statis, and “bile lakes.”

labs show: ↑alk phos & ↑conjugated bilirubin

A

secondary biliary cirrhosis

105
Q

both intra- and extrahepatic. Inflamation and fibrosis of bile ducts leads to alternating strictures and dilation with “beading” on ERCP.

A

Primary sclerosing cholangitis

106
Q

Primary sclerosing cholangitis us assiciated with ________

A

ulcerative colitis

107
Q

Primary sclerosing cholangitis can lead to _______

A

secondary biliary cirrhosis

108
Q

charcot’s triad of cholangitis

A

1) jaundice
2) fever
3) RUQ pain

109
Q

mildly ↓ UDP-glucuronyl transferase. Asymptomatic but unconjugated bilirubin is elevated without overt hemolysis. Associated with stress

A

Gilbert syndrome

110
Q

Absent UDP-glucuronyl transferase. Presents early in life; pts die within a few years.

A

Crigler-Najjar syndrome, type I

111
Q

Findings include: juandice, kernicterus (bilirubin deposition in brain), ↑ unconjugated bilirubin.

A

Crigler-Najjar syndrome, type I

112
Q

treatment of Crigler-Najjar syndrome, type I

A

plasmapheresis and phototherapy

113
Q

Crigler-Najjar type I is a severe dz. Type II is less severe and responds to _______

A

phenobarbital

114
Q

this d/o is due to conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign.

A

Dubin-Johnson syndrome.

115
Q

this syndrome is similar to Dubin-Johnson syndrome but even milder and does not cause black liver.

A

Rotor’s syndrome

116
Q

normally, liver cells convert unconjugated (indirect) bilirubin into _________ bilirubin

A

conjugated (direct)

117
Q

_______ is water soluble and can be excreted into urine

A

Direct bilirubin

118
Q

The liver converts some of the direct bilirubin into bile to be converted by gut bacteria to ________

A

urobilogen

119
Q

Some urobilogen is _______

A

reabsorbed.

120
Q

Some urobilinogen is also formed directly from ________

A

heme metabolism

121
Q

Give the jaundice type:
conjugated/unconjucated hyperbilirubinemia
↑ urine bilirubin
nml/↓ urine urobilinogen

A

hepatocellular jaundice

122
Q

Give the jaundice type:
conjugated hyperbilirubinemia
↑ urine bilirubin
↓ urine urobilinogen

A

obstructive jaundice

123
Q

Give the jaundice type:
unconjucated hyperbilirubinemia
no urine bilirubin
↑ urine urobilinogen

A

hemolytic jaundice

124
Q

deposition of hemosiderin (iron)

A

hemosiderosis

125
Q

dz caused by iron deposition

A

hemochromatosis

126
Q

classic triad of hemochromatosis

A

1) micronodular cirrhosis
2) pancreatic fibrosis
3) skin pitmentation

127
Q

hemochromatosis can lead to this autoimmune dz

A

“bronze” dbts

128
Q

hemochromatosis results in this heart condition

A

CHF

129
Q

increased risk of this CA with hemochromatosis

A

HCC

130
Q

primary hemochromatosis follows this inheritance pattern

A

autosomal recessive

131
Q

secondary hemochromatosis is due to this

A

chronic transfusion therapy

132
Q

Labs for this dz show ↑ ferritin, ↑ iron, ↓ TIBC which results in ↑ transferrin saturation

A

hemochromatosis

133
Q

tx hemochromatosis w/

A

phlebotomy, defoeroxamine

134
Q

this dz is due to inadequate hepatic copper excretion and failure of copper to enter circulation as ceruplasmin. It leads to copper acccumulation, especially in liver, brain, cornea, kidneys, joints. Itis also known as hepatolenticular degenration

A

Wilson’s dz

135
Q

what is the inherritance pattern of Wilson’s dz

A

autosoma-recessive

136
Q

how do you tx Wilson’s dz

A

penicillamine

137
Q

Wilsons dz is characterized by:

ABCD

A

Asterixis
Basal ganglia degeneration (parkinsonian symptoms
↓Ceruplasmin, Cirrhosis, Corneal deposits (Kayser-Fleischer rings), Copper accumulation, Carcinoma (hepatocellular, Choreiform movements
Dementia

138
Q

this syndrome is due to occlusion of IVC or hepatic veins with centrilobular congestion & necrosis, leading to congestive liver dz (hepatomegaly, ascites, abdoinal pain, and eventual liver failure). It is associated with polycythemia vera, pregnancy, hepatocellular carcinoma

A

Budd-Chiari syndrome

139
Q

This dz shows swollen and necrotic hepatocytes, neutorphil infiltration, mallory bodies, fatty change, and sclerosis around the central vein. SGOT (AST) to SGPT (ALT) ratio is usually >1.5

A

alcoholic hepatitis

mneu: A Scotch and Tonic:
AST elevated (>ALT) w/ alcoholic hepatitis

ALT> AST in viral hepatitis

140
Q

Cirrho (greek) =

A

tawny yellow

141
Q

in portal hypertension esophageal verices can lead to these 2 things

A

hematemesis and melana

142
Q

in portal hypertension peptic ulcers can lead to

A

melana

143
Q

splenomegly, caput medusae, ascites, hemorrhoids, esophageal veraces, melana are all symptoms of

A

portal hypertension

144
Q

coma, scleral icterus, fetor hepaticus (bad breath), spider nevi, gynomastia, jaundice, loss of sexual hair, asterixis (coarse hand tremor), increased PTT, anemia, ankle edema, are effects of this

A

effects of liver cell failure

145
Q

in cirrhosis there is diffuse _____ of liver, which destoys normal architecture

A

fibrosis

146
Q

in cirrhosis there is nodular regeneration. Micronodular nodules (<3mm) tend to be due to _______

A

metabolic insult (e.g.,e alcohol, hematochromatosis, Wilson’s dz)

147
Q

in cirrhosis there is nodular regeneration. Macronodular nodules (>3mm) tend to be due to _______

A

post infectious or drug induced hepatitis

148
Q

these nodules represent an increased risk for what CA?

A

HCC

149
Q

A portacaval shunt between these 2 vv may relieve portal hypertension

A

splenic vv & L renal vv

150
Q

this is the 3rd most common CA. Risk factors include: colorectal villous adenomas, chronic inflammatory bowel dz, high fat and low fiber diets, increaed age, familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal CA (HNPCC), DCC gene deletion, & + family hx.

A

colorectal CA

151
Q

What is Peutz-Jeghers? Is it a risk factor for colorectal CA?

A

a benign polyposis syndrome

not a risk factor

152
Q

who and how do you screen for colorectal CA

A

pts >50 w/ stool guiac, and colonoscopy

153
Q

this is visualized on barium swallow x-ray as “apple core” lesion”

A

colorectal CA

154
Q

this is a nonspecific tumor marker for colorectal CA

A

CEA

155
Q

this is a congenital megacolon characterized by lack of enteric nervous plexus in a segment (Auerbach’s and Meissner’s plexuses) due to failure of neural crest and cell migration It presenta as chronic constipation early in life.

A

Hirschsprung’s dz

mneu: think of a giant spring that has SPRUNG in the colon

156
Q

in hirschrung’s dz the dialated porion of the colon proximal to the aganglionic segment is called ________

A

transition zone

157
Q

pts w/ this syndrome are at increased risk for hirschrung’s dz

A

downs syndrome

158
Q

“telescoping” of 1 bowel segment into distal segment; can compromise the blood supply. Often due to intraluminal mass

A

Intussuption

159
Q

twisting of portion of bowel around its mesentery; can lead to obstruction and infection. May occur at sigmoid colon, where there is redundant mesentery

A

Volvulus

160
Q

blind pouch leading off the alimentary tract, lined by mucosa, muscularis, and serosa, that communicates with the lumen of the gut

A

diverticulum

161
Q

this type of diverticulum consists of an outpouching of all 3 gut wall layers

A

true diverticulum

162
Q

In this type of diverticulum, only the mucosa and submucosa outpouch

A

false diverticulum

163
Q

this type type of diverticulum occurs especially where vasa recta perforate the muscularis externa

A

false diverticulum

164
Q

Most diverticula are aquired are termed “false” in that they lack what

A

muscularis externa

165
Q

most false diverticula exist where?

A

sigmoid colon

166
Q

many diverticula is refered to as ________

A

diverticulosis

167
Q

prevelence of diverticulosis in pts >60 is ~ ________.

A

50%

168
Q

this condition is caused by increased intraluminal pressure and focal weakness in the colonic wall

A

diverticulosis

169
Q

diverticulosis most frequently involves what part of the GI tract?

A

sigmoid colon

170
Q

diverticulosis is associated with what type of diet?

A

low fiber

171
Q

give common presenting symptoms of diverticulosis

A

asymptomatic or associated with vague discomfort and/or rectal bleeding

172
Q

this is an inflammation of diverticula classically causing LLQ pain. It may lead to perforation, peritonitis, abscess fromation, or bowel stenosis.

A

diverticulitis

173
Q

pt presents w/ initial diffuse periumbilical pain that then becomes localized to pain at McBurney’s point. Nausea and fever may accompany.

A

appendicitis

174
Q

while this occurs in all age groups it is the most common indication for emergent abdominal surgery in children

A

appendicitis

175
Q

appendicitis may perferate and become what?

A

peritonitis

176
Q

important d/d of appendicitis in the elderly

A

divrticulitis

177
Q

important d/d of appendicitis in women of childbering age

A

ectopic pregnancy

178
Q

women of childbering age presents w/ pain that may be appendicitis or may be ectopic pregnancy–what is you’re next step.

A

order B-hCG to r/o ectopic

179
Q

two most common types of inflammatory bowel dz

A

crohn’s dz, ulcerative colitis

180
Q

possible etiology of crohn’s

A

infectious

181
Q

possible etiology of ulcerative colitis

A

autoimmune

182
Q

location of crohn’s

A

may involve any portion of GI, usually involves the TERMINAL ILIUM and colon. SKIP LESIONS. RECTAL SPARING

mneu: For CHROHN’S,think of a FAT GRANny and an old CRONE SKIPPING down a COBBLESONE road away from the WRECK (rectal sparing)

183
Q

location of UC

A

COLITIS=colon inflamation. CONTINUOUS. ALWAYS RECTAL INVOLVEMENT.

184
Q

Gross morphology of this IBD includes transmural inflammation. COBBLESTONE mucosa, creeping FAT, bowel wall thickening (“string sign” on barium swallow x-ray), linear ulcers, fissures, fistulas

A

CD

mneu: For CHROHN’S,think of a FAT GRANny and an old CRONE SKIPPING down a COBBLESONE road away from the WRECK (rectal sparing)

185
Q

Gross morphology of this IBD includes mucosal and submucosal inflammation only. Friable mucosal pseudopolyps with freely hanging mesentery

A

UC

186
Q

Microscopic morphology of this IBD includes noncaseating GRANulomas and lymphoid aggregates.

A

CD

mneu: For CHROHN’S,think of a FAT GRANny and an old CRONE SKIPPING down a COBBLESONE road away from the WRECK (rectal sparing)

187
Q

on mircroscopic morphology this IBD, shows crypt absesses and ulcers, bleeding, no granulomas

A

UC

188
Q

complications of this IBD includes strictures, fistulas, perianal dz, malabsorption, nutritional depletion

A

CD

189
Q

complications of this IBD includes severe stenosis, toxic megacolon, COLORECTAL CARCINOMA

A

UC

190
Q

extraintestinal manifestations of this IBD includes migratory polyartheritis, erythema nodosum, ankylosing spondylitis, uveitis, immunologic disorders

A

CD

191
Q

extraintestinal manifestations of this IBD includes pyoderma gangrenosum. Primary sclerosing cholangitis

A

UC

192
Q

this type of CA is associated w/ dietary nitrosamines, achlorhydria, and chronic gastritis.

A

stomach CA

193
Q

stomach CA is almost always this type of CA

A

adenocarcinoma

194
Q

Stomach CA has early aggressive local spread to to the LN & this location.

A

liver

195
Q

Stomach CA is turmed this when it is diffusely infiltrative w/ a thickened, rigid appearance.

A

linitis plastica

196
Q

what is Virchow’s node

A

mets from stomach to supraclavicular node

197
Q

what is Krukenberg’s tumor

A

bilateral mets to ovaries

198
Q

Krukenberg’s tumor is characterized by abundant mucus and these type of cells

A

“signet ring” cells.

199
Q

in Gastric ulcers pain is ________(greater or lesser) with meals

A

Greater - often results in weight loss

200
Q

in Duodenal ulcers pain is ________(greater or lesser) with meals

A

lesser-often results in weight gain

201
Q

H pylori is _____% in gastric ulcers and ______% in duodenal ulcers

A

G-70%

D-~100%

202
Q

this type of ulcer is due to DECREASED MUCOSAL PROTECTION against gastric acid

A

Gastric ulcer

203
Q

this type of ulcer is due to INCREASED GASTRIC SECRETION OR DECREASED MUCOSAL PROTECTION

A

Duodenal ulcer

204
Q

associated with hypertrophy of Brunner’s glands

A

duodenal ulcer

205
Q

tend to have clean, “punched-out” margins unlike the raises/irregular margins of carcinoma.

A

duodenal ulcers

206
Q

give 2 potential complications of duodenal ulcers (2)

A

bleeding, penetration, perforation, and obstruction.

207
Q

“triple therapy” for H pylori.

A

metronidazole, bismuth salicylate, and either amoxicillinn or tetracycline with or without a PPI.

208
Q

incidence of peptic ulcer is 2ce in this group of people

A

smokers

209
Q

disruption of mucosal barriers leads to inflammation

A

acute gastritis

210
Q

acute gastritis is ______ (erosive or nonerosive)

A

erosive

211
Q

chronic gastritis is ______ (erosive or nonerosive)

A

nonerosive

212
Q

give 3 causes of acute gastritis

A

stress, NSAIDs, etoh, uricemia, burns, and brain injury

213
Q

this type of ulcer is caused by burns

A

Curling’s ulcer

214
Q

this type of ulcer is caused by brain injuury

A

cushing’s ulcer

215
Q

what are the 2 types of chronic gastritis

A

type A -fundal

type B- antral

216
Q

this type of chronic gastritis is caused by an autoimmune d/o characterized by autoantibodies to parietal cells, pernicious anemia, and Achlorhydria

A

type A-fundal

mneu: type A=4As

217
Q

this type of chronic gastritis is caused by H. pylori infection

A

type B-antral

mneu: Type B= a Bug, H. pylori

218
Q

Both types of chronic gastritis carry an increased risk of this

A

gastric carcinoma

219
Q

this results from glandular (columnar epithelial) metaplasia–replacement of nonkeratinized squamous epithelium with gastric (columnar) epithelium in the distal esophagus. Due to chonic acid reflex.

A

Barrett’s esophagus

mneu: BARRett’s = Becomes Adenocarcinoma, Results from Reflux

220
Q

give the common dx from the labs:

ALT>AST

A

viral hepatitis

221
Q

give the common dx from the labs:

ALT<AST

A

alcoholic hepatitis

222
Q

give the common dx from the labs:

AST only

A

MI

223
Q

this is elevated in various liver dz

A

GGT (gamma glutamyl transpeptidase)

224
Q

give the common dx from the labs:

elevated alk phos

A

obstructive liver dz (HCC)

bone dz

225
Q

give the common dx from the labs:

increased Amylase

A

acute pancreatitis, mumps

226
Q

give the common dx from the labs:

increased Lipase

A

Acute pancreatitis

227
Q

decreased Ceruloplasmin

A

Wilson’s dz

228
Q

Most common congenital anomaly of the GI tract. persistence of the vitelline duct or yolk stalk

A

merkel’s diverticulum

229
Q

cystic dilation of vitelline duct

A

omphalomesenteric cyst

230
Q

this may contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue

A

merkel’s diverticulum

231
Q

Give the 5 2s of Merkel’s diverticulum

A
2 in. long
2 feet from ileocecal valve
2% of population
presents 2st 2 yrs of life
may have 2 types of epithelia
232
Q

failure of relaxation of lower esophageal sphincter due to loss of myenteric (Auerbach’s plexus

A

Achalasia

233
Q

Causes progessive dysphagia. Barium swallow shows dilated esophagus w/ an area of distel stenosis.(“Bird Beak” on barium swallow.)

A

Achalasia

234
Q

A-chalasia means

A

absense of relaxation

235
Q

achalasia is associated with an increased risk of this.

A

esophageal carcinoma

236
Q

Secondary achalasia may arise from this dz

A

Chagas’ dz

237
Q

protrusions of peritoneum through an opening, usually sites of weakness

A

abdominal hernia

238
Q

in this type of hernia abdominal sx enter the thorax. it may occur in infants as a result of defective development of pleuroperitoneal membrane

A

diaphragmatic hernia

239
Q

this is the most common diaphragmatic hernia, in which the stomach herniates upward through the esophageal hiatus of the diaphram

A

hiatal hernia

240
Q

This type of hernia goes through the INternal (deep) inguinal ring and external (superficial) inguinal ring and INto the scrotum.

A

Indirect inguinal hernia

241
Q

This type of hernia bulges directly throgh the abdominal wall medial to inferior epigastric artery.

A

direct

MDs don’t LIe:
Medial to inferior epigastric artery=Direct hernia
Lateral to inferior epigastric artery=Indirect hernia

242
Q

This type of hernia enters the inguinal ring lateral to inferior epigastric artery.

A

indirect

MDs don’t LIe:
Medial to inferior epigastric artery=Direct hernia
Lateral to inferior epigastric artery=Indirect hernia

243
Q

Indirect hernias occur in ______ owing to failure of processus vaginalis to close. They are much more common in males

A

infants

244
Q

this type of hernia protrudes through the inguinal (Hesselbach’s)triange. It goes through the external (superficial inguinal ring only. It often occurs in older men.

A

direct inguinal hernia

245
Q

abdominal hernias [pic.p.273]

A

1) inferior epigastric vessels
2) rectus abdominus mm
3) inguinal (Poupart’s ligament)
4) direct inguinal hernia (through hesselbach’s triangle)
5) indirect inguinal hernia

246
Q

hesselbach’s triangle includes:

A

1) inferior epigastric aa
2) lateral border of rectus abdominis
3) inguinal ligamnent

247
Q

what is bile composed of (6)

A
bile salts
cholesterol
phospholipids
bilirubin
water
ions
248
Q

what are bile salts

A

bile acids conjugated to glycene or taurine to make them water soluable

249
Q

this is a product of heme metabolism

A

bilirubin

250
Q

bilirubin is actively taken up by these cells

A

hepatocytes

251
Q

this type of bilirubin has been conjugated with glucuronic acid and is water soluble

A

direct bilirubin

252
Q

this type of bilirubin is water insoluble

A

unconjugated

253
Q

this describes yellowign of the skin and sclera as a result of elevated bilirubin levels

A

jaundice

254
Q

apical surface of hepatocyts face ________

basolateral surface face ________

A

bile canaliculi

sinusoids

255
Q

in carbohydrate digestion only this type of molecule is absorbed

A

monosaccaride (glucose, fructose, galactose)

256
Q

this amylase starts digestion, it hydrolyzes alpha-1-4 linkages to yield disaccharides (maltose, maltotriose, and alpha-limit dextrans).

A

salivary amylase

257
Q

this amylase is in highest concentration in duodenal lumen, it hydrolyzes starch to oligosaccharides and disaccarides

A

pancratic amylase

258
Q

this amylase is at the brush border of intestines. It is the rate-limiting step in carbohydrate digestion. It produces monosaccarides from oligo-and disaccharides

A

oligosaccharide hydrolases

259
Q

name the portion of the GI tract where the following substances would be absorbed:

etoh

A

stomach

260
Q

name the portion of the GI tract where the following substances would be absorbed:

glucose via Na+cotransporter
vit A & D
Fatty acids
Iron 
Ca++
A

duodenum

261
Q

name the portion of the GI tract where the following substances would be absorbed:
glucose, galactose, monosaccharides, disaccharides, vit A & D
Fatty acids,
PROTIENS and AMINO ACIDS

A

proximal Jejunum

262
Q

name the portion of the GI tract where the following substances would be absorbed:

WATER SOLUBLE VITAMENS
disaccharides
fatty acids
proteins and amino acids

A

terminal jejunum

263
Q

name the portion of the GI tract where the following substances would be absorbed:

protiens and amino acids
VIT B12
BILE SALTS
*acts as a reserve can absorb additonal nutrents if required

A

Ileum

264
Q

name the portion of the GI tract where the following substances would be absorbed:

H2O
K+
NaCl
Short chain fatty acids

A

Colon

265
Q

Give the 4 glands that secrete saliva

A

parotid, submandibular, submaxillary, and sublingual

266
Q

this component of saliva begins starch digestion. It is inactivated by low pH upon reaching the stomach

A

alpha-amylase (ptalin)

267
Q

this component of saliva neutralizes oral bacterial acids and maintains dental health

A

bicarbonate

268
Q

this component of saliva lubricates food

A

mucins (glycoproteins)

269
Q

salivary secretion is stimulated by what?

A

autonomics-sympathetic & parasympathetic

270
Q

sympathetic secretion of saliva occurs via this ganglion?

A

Superior cervical ganglion (T1-T3)

271
Q

parasympathetic secretion of saliva occurs via these nerves?

A

facial & glossopharyngeal

272
Q

with a low flow rate of saliva(sympathetic)expect this type of saliva

A

hypotonic

273
Q

with a high flow rate of saliva(parasympathetic)expect this type of saliva

A

isotonic

274
Q

intrinsic factor comes from these cells in what part of the GI

A

parietal cells of the stomach

275
Q

the action of this GI secretory product is to function as a vit B12 binding protien which is required for B12 uptake in terminal ileum

A

intrinsic factor

276
Q

autoimmune destruction of parietal cells results in what 2 conditions

A

chronic gastritis and pernicious anemia

277
Q

gastric acid comes from what cells in what part of the GI tract

A

parietal cells of the stomach

278
Q

what is the action of gastric acid

A

lower stomach pH

279
Q

histimine, ACh, and gastrin act to ____ secretion of gastric acid

A

increase

280
Q

somastatin, GIP, prostaglandin, secretin act to ___secretion of gastric acid

A

decrease

281
Q

Pepsin is secreted by what cells in what part of the GI tract

A

chief cells of the stomach

282
Q

pepsin functions how

A

protien digestin

283
Q

what pH is the optimal fx of pepsin

A

1-3

284
Q

pepsin production is ___ by vagal stimulation and local acid

A

increased

285
Q

inactive pepsinogen is convertid to pepsin by _____

A

H+

286
Q

HCO3- is produced by these cells in these 2 parts of the GI tract

A

mucosal cells in the stomach and duodenum

287
Q

the fx of this GI secretory product is to neutrolize acid and prevent autodigestion

A

HCO3-

288
Q

HCO3 release is stimulated by this?

A

secretin

289
Q

gastrin is produced by these cells in this part of the stomach

A

G cells

antrum

290
Q

this GI secretory product acts to increase gastric H+ secretion, increae growth of gastric mucosa, and increase gastric motility

A

gastrin

291
Q

gastrin release is ____ by stomach distension, amino acids, peptides, vagal stimulation

A

increased

292
Q

gastrin release is ____ by H+ secretion and stomach acid pH<1.5

A

decreased

293
Q

gastrin release is increased in this CA

A

Zollinger-Ellison syndrome

294
Q

phenylalanine and tryptophan are potent stimulators of this hormone

A

gastrin

295
Q

Where is Cholescystokinin released from? Give cells and GI location.

A

I cells
duodenum
jejunum

296
Q

this GI secretory product acts to increase pancreatic secretion, increase gallbladder contraction; decrease gastric emptying, increase growth of exocrine pancrease and gallbladder

A

Cholescystokinin (CKK)

297
Q

cholecystokinin is ___ by secretin ans stomach pH <1.5

A

decreased

298
Q

cholecystokinin is ___ by fatty acids and amino acids

A

increased

299
Q

In cholelthiasis, pain worsens after fatty food ingestion due to this

A

increased CCK

300
Q

What cells and GI location is secretin from

A

S cells

duodenum

301
Q

what is the action of secretin

A

increased pancreatic HCO3- secretion and decreased gastric acid secretion

302
Q

secretin is ___ by acid, and fatty acids in the lumen of the duodenum

A

inceased

303
Q

increased HCO3- neutralizes gastric acid in the duodenum, allowing these enzymes to function

A

pancreatic

304
Q

where does somatostatin come from? give the cell and the GI location

A

D cells in the pancreatic islets and GI mucosa

305
Q

this GI secretory product acts to decrease gastric acid and pepsinogen secretion, decrease pancreatic and small indestine fluid secretion. decrease gallbladder contraction. decrease insulin and glucagon release

A

somatostatin

306
Q

somatostatin is ____ by acid ____ by vagal stimulation

A

increased

decreased

307
Q

this hormone is considered an inhibitory hormone with antigrowth effects (digestion and absorption of substances are needed for growth)

A

somatostatin

308
Q

Where is gastric inhibitory peptide released from. Give the cell and the location in the GI.

A

K cells

duodenum and jejunum

309
Q

what is the exocrine fx of of GIP

A

decrease gastric acid secretion

310
Q

what is the endocrine fx of of GIP

A

increase insulin release

311
Q

GIP is ____ by fatty acids, amino acids, & oral glucose.

A

increaed

312
Q

this is the only GI hromone stimulated by all three nutrient glasses (amino acids, & oral glucose)

A

GIP

313
Q

why is an oral glucose load used more rapidly than the equivalent given by IV

A

GIP

314
Q

cholecystokinin is ___ by secretin ans stomach pH <1.5

A

decreased

315
Q

cholecystokinin is ___ by fatty acids and amino acids

A

increased

316
Q

In cholelthiasis, pain worsens after fatty food ingestion due to this

A

increased CCK