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Flashcards in Exam 1 Deck (423):
1

does esophagus have serosa?

upper esophagus = no serosa

lower esophagus = serosa (intraperitoneal)

2

oral mucosa histological characteristics/layers

1. stratefied squamous unkeratinized/lightly keratinized epithelium
2. underlying CT - lamina propria with BVs

3

saliva contents (4)

1. secretory IgAs
2. beta defensins from epithelial cells (antibacterial)
3. amylases
4. lysosyme

4

tongue histology features (5)

1. strategied squamous unkeratinized/slightly keratinized

2. papillae (mostly filiform, some fungiform, few circumvallate papillae at root of tongue with taste puds, foliate papillae on lateral surface with taste buds and serous glands)

3. lots of skeletal muscle (intrinsic and extrinsic)

4. minor salivary glands (mixed or either or, associated with folate and circumvalate)

5. lingual lymph nodes (GALT)

5

difference between the nuclei of supportive and sensory cells in taste buds

sensory have rounder, lighter stained nuclei,

supportive have darker and more elongated nuclei

6

what tastes can you detect

sugar
salt
bitter
sour
umami

7

are sensory cells attached to myelnated or unmyelinated nerve fibers

myelinated

8

minor salivary glands are where

all over oral cavity

9

what are major salivary glands (what are they made of)

1. parotid (mostly serous - amylase, proteinaceous)
2. submandibular (mix of serous and mucous)
3. sublingual (mostly mucous acini)

10

mucous vs serous characteristics

mucous is lighter than serous

11

ducts

intercalated to striated to interlobular and main excretory

12

what makes enamel

ameloblasts

13

what is deep to enamel

dentil, which is vital, innervated, and bone-like

14

what secretes dentin

odontoblasts. odontoblasts processes radiate throughout dentin in dentinal tubules, like osteocyte processes in canaliculi of bone

15

how many teeth to children have

20 primary teeth

16

which teeth are lost first to last

1. central incisors
2. lateral incisors
3. first molar
4. canine
5. second molars

17

how many teeth do adult have

32

18

tooth development stages

1. ectoderm thickens as dental lamina
2. invaginates due to inducement of NCC mesenchyme called dental pipilla

19

what do NCC develop in teeth

odontoblasts (dentin) and pulp of tooth

20

what does ectoderm form in teeth

ameloblasts (enamel)

21

oropharynx histologic characteristics (4)

1. SS uK epithelium
2. lamina propria
3. submucosa with lymphoid follicles
4. skeletal muscle in walls

22

how long is the human GI tract

30 feet

23

myenteric is associated with what layer

muscular

24

auerbach is associated iwth what layer

muscular - myenteric = auerbach

25

meissner's plexus is associated iwith what layer

submucosal

26

myenteric stimulation causes (4)

motility:
1. increases tone,
2. contraction intensity,
3. contraction rate,
4. speed of conduction)

27

submucosal stimulation causes (3)

secretion and absorption:
1. integration of signals
2. local contraction

28

what does NOT count as research (2)

1. undisciplined or systematic
2. doesn't seek to add to body of knowledge

29

tenants of nurenburg code (3)

1. voluntary consent
2. benefits outweigh risk
3. participates can terminate at any time

30

declaration of Helsinki

international standard for biomedical research ethics - interest of subject must prevail over the interest of science

31

belmont principles (3)

1. respect for persons
2. beneficience
3. justice

32

respect for persons

individual autonomy, protection of individuals with reduced autonomy)

33

beneficence

maximize benefits and minimize harms

34

justice

equitable distribution of research costs and benefits

35

C.A.G.E. interview

for alcohol dependence

1. ever had to cut down
2. annoyed when people tell you to quit?
3. guilt
4. need eye opener

for women - does it take more and more alcohol to get you drunk

36

mesolimbic circuit

goes from ventral tegmental to nucleus accumbens -- reward circuit, mediated by dopamine and endorphins

37

alcohol's affect on arousal and sleep circuit

alcohol suppresses brainstem mechanisms for rapid heart rate etc. and withdrawal can cause seizures etc - over-excitation

38

aeclaspian authority

tell your patients the health adverse effects

39

naltrexone

blocks endorphin mediated sensation of reward- reduces craving

40

topiramate

reduces appetitive behavior - food or drink

41

most of vagus is afferent or efferent?

afferent - receiving signals

42

short reflex pathway

entirely within enteric system causing stimulus and response (change in motility or secretion)

43

long reflex pathway

involve sympathetic ganglia and transmit signals to other parts - including vago-vasal pathway

44

the enteric nervous system produces most of the bodies ____ neurotransmistter

seratonin -95%

45

what does Ach do in GI tract (3)

1. contracts SM
2. relax sphincters
3. increase secretion (salivary, gastric and pancreatic)

46

what does NE do in the GI tract (3)

1. relax SM
2. contract sphincter
3. enhance salivary secretion

47

what does VIP do in the GI tract

relax SM

48

what does NO do in the GI tract

relax SM

49

What does GRP do in the GI tract

increase gastric secretion

50

cephalic phase of digestion

1. Sight, smell, thought of food relays info to dorsal vagal complex
2. vagovagal reflex triggers secretory and motor behavior in stomach -- releases GRP (triggers G cells to release of gastrin which activates parietal and chief cells) and ACh (to inhibit somatostatin)

51

what is the stimulation for salivation (hormonal, paracrine etc.)

neurocrine

52

is saliva acidic or basic?

alkaline

53

why is bicarb secretion necessary in saliva

to protect from gastric acid reflux

54

what does amylase do

initiates startch digestion

55

what does lingual lipase do

picks up slack from pancreas in triglyceride digestion

56

stages of salivary secretion (2)

1. acinar cells secrete isotonic primary saliva (amylase +/- mucin)
2. ductal cells make saliva alkaline (sodium and chloride reabsorb, potassium and bicarb secrete) - low perm to water -- makes saliva hypotonic

57

things that stimulate saliva secretion (4)

1. conditioning (pavlov)
2. food
3. nausea
4. smell

58

things that inhibit saliva secretion (4)

1. dehydration
2. fear
3. sleep
4. anticholinergic drugs (atropine)

59

what happens to saliva glands if you cut the vagus

decreased secretion (Same with cut sympathetic) but ALSO get glandular atrophy

60

what can you measure clinically in saliva? (5)

1. biomarkers
2. steroid levels (free not bound)
3. viral infections (HIV, hepC, EBV)
4. bacterial (H. pylori)
5. drug levels

61

phases of swallowing

1. voluntary
2. pharyngeal (controlled by swallowing center in medulla)
3. esophageal

62

when breathing, is UES open or closed?

closed

63

when swallowing, is UES open or closed?

open, and glottis is closed

64

4 layers of GI tract histology

1. mucosa (epithelium, lamina propria, muscularis mucosae)
2. submucosa (BVs, folds)
3. muscularis externa (inner circular, outer longitudinal)
4. adventitia (if retroperitoneal) serosa (if introperitoneal)

65

what in GI is derived from spanchnic mesoderm (4)

1. lamina propria
2. submucosal CT
3. muscularis externa
4. adventitia

66

what in gI is derived from regular mesoderm

lymphoid tissue - from bone marrow - GALT

67

what is the derivation for liver/pancreas parenchymal cells

endoderm

68

foregut is from where to where

buccopharyngeal membrane (stomodial) to anterior intestinal portal

69

midgut is from where to where

from anterior to posterior intestinal portal

70

hindgut is from where to where

from posterior intestinal portal to coacal memrane

71

lower foregut is supplied by what

celiac trunk

72

midgut is supplied by what

superior mesenteric artery

73

hindgut is supplied by what

inferior mesenteric artery

74

cranial foregut derivatives (6)

1. epithelium in posterior oral cavity
2. respiratory diverticulum
3. auditory tube epithelium
4. palatine tonsilar crypt epithelium
5. parathyroid epithelium
6. thymus epithelium

75

caudal foregut derivatives (4)

1. oropharynx and esophagus epithelium
2. stomach epithelium
3. first part of duodenum epithelium
4. liver, pancreas, gall bladder and duct epithelium

76

midgut derivatives (5)

1. second part of duodenum
2. ileum and jejunum
3. cecum and vermiform appendix
4. ascending colon
5. transverse colon to approximate middle

77

hindgut derivatives (5)

1. second half of transverse colon
2. descending colon
3. sigmoid colon
4. rectum
5. anal canal to anal valves (pectinate line)

78

gastric rotations

1. first, rotates dorsal to ventral and elongates over to form greater omentum

2. second rotation brings cardiac portion inferiorly to the left, and pyloric superiorly and to the right

79

septum transversum and liver

liver diverticulum grows into septum transversum mesoderm and branches, but remains connected

80

what is the rotation of the midgut and what's the axis of rotation

270 degrees counter clockwise

axis of rotation is formed by vitelline duct and superior mesenteric artery

81

secondarily retroperitoneal

becomes plastered to body wall
1. pancreas
2. part of duodenum
3. ascending colon
4. descending colon

82

do you have sensation above pectinate line?

no

83

where would a carcinoma above the pectinate line drain into

inferior mesenteric nodes

84

where would a carcinoma below the pectinate line drain into

superficial inguinal nodes

85

epithelial changes at pectinate line

simple columnar to stratefied squamous unkeratinized

86

pyloric stenosis cause (2)

congenital defect - due to hypertrophy of pyloric sphincter

also early exposure to erythromycin

87

clinical finding of pyloric stenosis

projectile vomiting in newborns - curdled milk (no bile)

88

pyloric stenosis treatment (2)

reducing muscular layers and with atropine

89

ileal diverticulum incidence

most common congenintal GI defect 2%

90

ileal diverticulum description

remnant of vitelline duct, finger like projection toward end of midgut - ileum

91

clinical presentation of ileal diverticulum

often astymptomatic, but if it contains atopic gastric or pancreatic tissue, you will get ulceration

92

omphalocele description

defect in anterior abdominal wall covered by peritoneum and amnionic sac - failed retreat of midgut loop

93

gastrochisis

raw exposed bowel loops - can disinguish in utero from omphalocele via sonogram

94

congenital megacolon

neural crest cells don't populate a certain area of the colon (aganglionic segment), resulting in no myenteric plexus and poor motility

95

parietal cells secrete

hydrochloric acid

gastric intrinsic factor (for B12)

96

what do chief cells secrete

pepsinogen

97

where do you find villi

only small intestine

98

where do you find crypts

in stomach, small and large intestines

99

histological characteristics of esophagus from epithelium to muscularis externa (5)

1. stratefied sqamous unkeratinized epithelium
2. submucosal folds
3. submucosal mucous glands
4. muscularis mucosae
5. thick inner circular and outer long (upper third skeletal, middle mixed, lower smooth)

100

barret esophagus

reflux of gastric contents causes changes of esophageal epithelium to look more like small intestinal epithelium - metaplasia. can then undergo malignant hyperplasia

101

hiatal hernia

stomach can project up through the diagraph - end up getting chronic reflux because the sphincter doesn't work well

102

esophageal varices

alcoholics
vessels get dilated and varicosed by constant irritation. have difficulty swallowing food

103

general stomach histological layers from in to out (5)

1. pitted - mucosal gastric pits (faveoli) NO VILLI.
2. epithelium has many cell types
3. rugae - transient submucusal folds
4. muscularis externa has 2-3 poorly defined layers
5. serosa - intraperitoneal

104

cardiac stomach specific findings (3)

1. gastric pits are short
2. only mucous cells
3. absolute thickness is less

105

fundic/corpic stomach specific findings (5)

1. much thicker
2. pits have variety of cell types and are deeper
3. mucous cells on surface and neck
4. acidophilic parietal cells by neck
5. deeper basophilic chief cells

106

pyloric stomach specific characteristics (3)

1. lymphoid tissue
2. fewer parietal and chief, more mucous cells
3. still thick

107

where are stem cells in gastric pit

in the neck and isthmus

108

what makes parietal cells acidophilic?

mitochondria

109

what stimulates parietal cells

gastrin - get more boarder with proton pump

110

what starts being broken down in stomach

proteins and lipids

111

duodenum histological layers (5)

1. villi
2. crypts of libercuhn
3. submucosal brunner glands (bicarb and mucous for protection)
4. inner circular outer long muscularis external
5. some parts secondarily retroperitoneal with adventitia, some intraperitoneal with serosa

112

what are submucosal folds in small intestine called

plicae ciruclaris, they all have villi on them, and the folds are permanent

113

where are lacteals and what do they do

in lamina propria absorb lipids

114

what do paneth cells do and where are they

at bases of crypts

secrete antimicrobial protesins like lysosome, defensins and immunoglobulins

115

what do paneth cells look like

acidophilic - bright red granules

116

what are M cells

epithelial cell type that are antigen presenting (like macrophages) present to lymphocytes - overlie peyer's patches in Ileum

117

enteroendocrine cells - what do they do, what basic 2 kinds are there

secrete regulatory hormones - can be open (access to lumen) or closed

118

G cells - where are they

stomach mostly

nerve fibers reselase Ach with distension, Ach stimulates G cells to secrete gastrin (which then activates HCl secretion from parietal cells)

119

What do D cells do

secrete somatostatin (which is inhibitory to secretion)

120

Zollinger Ellison Syndrome presentation

abdominal pain, diarrhea and fatty stool, duodenal ulcers

121

what causes Zollinger Ellison

tumor causing too many G cells -- too much gastrin - -too much acid -- mucosal ulceration in stomach

122

what to do for Zollinger Ellison

resection and proton pump inhibitors (omeprazole)

123

brain-gut axis and eating disorders

ingested tryptophan becomes serotonin

psychotropic drugs modify seratonin, which benefits binge eating, not anorexia

124

DSM5 criteria for anorexia nervosa

1. significantly low body weight
2. persistent behavior that interferes with gaining weight
3. persistent lack of recognition of the seriousness/disturbance in one's body image

125

examples of compensatory behavior in bulimia nervosa (4)

1. fasting
2. vomiting
3. laxatives
4. exercise

126

DSM5 criteria for bulemia nervosa

1. recurrent episodes of binge eating - lack of control
2. compensatory behavior
3. binge-purge cycle at least once a week for 3 months

127

DSM5 criteria for binge eating

1. large amounts over short time (2 hours)
2. 1x/week

128

SCOFF screenint

1. do you make yourself Sick because you're so full
2. do you worry you have lost Control
3. have you lost more than One stone (14lbs) in past 3 months
4. do you believe yourself to be Fat when others believe you are thin
5. would you say Food dominates your life

129

demographic for avoidant
restrictive food intake disorder

children mostly

130

approved medication for bulemia nervosa

fluoxetine (prozac)

131

intestinal feedback with stomach (3)

1. positive feedback via gastrin released by duodenal mucosa
2. negative feedback of acid secretion via vagally mediated secretin release from S cells
3. negative feedback of gastrin release via paracrine mediated somatostatin release from D cells

132

how fast is duodenal pacemaker

12 slow waves per minute

133

how fast is ileal pacemaker

8 slow wakes per minute

134

orad vs aborad

orad is closer to mouth
aborad is further from mouth

135

NO, Ach and VIP - what causes contraction and relaxation of LES

Ach = contraction
VIP and NO = relaxation

136

Achalasia

inability of LES to relax - issue with enteric nervous system

137

examples of drugs that cause relaxation of LES tone (3)

1. nitroglycerine
2. beta blockers
3. calcium channel blockers

138

what sets BER

pacemaker cells in stomach - interstitial cells of Cajal

waves of membrane potential propagated by Na/K movement

139

action potentials in gut motility driven by what ion

calcium influx (somewhat sodium too)

140

motility during fasting

MMC (migrating motor complex)
- housekeeping function - cleans out gut

141

phases of MMC

1. quiescent
2. intermittent motor activity
3. repetitive contractions (lasts 5 min)

142

what hormone dictates MMC

motilin

143

where is the majority of fluid absorbed in GI tract

small intestine

144

is mucus acidic or basic

basic

145

cephalic phase accounts for what percent of gastric secretion with meal

30%

146

which part of stomach grinds food

antrum

147

what does acid environment of stomach do enzymatically

enables activation of pepsinogen to pepsin, which in turn begins protein digestion and co-secretes lipase

148

what happens when food enters duodenum (2)

1. stretch receptors send local feedback to fundus to further relax via NO and VIP
2. CCK feeds back to dorsal vagal center to further relax proximal stomach

149

when does pyloric sphincter open, and how much does it open

opens with secondary contractions in stomach, and allows for particles smaller than 1mm to exit stomach

150

where in stomach are G cells located

antrum

151

where in stomach are parietal cells located

fundus

152

where in stomach are chief cells lcoated

fundus

153

where in stomach are D cells located

antrum

154

where in stomach are ECL cells located

fundus

155

where are oxyntic glands

body/fundus

156

what triggers gastrin release (3)

1. stretch
2. vagus
3. products of digestion - peptides amino acids

157

what triggers somatostatin release

1. H+

158

at what pH is pepsinogen cleaved

less than 3.5

159

GRP

releases gastrin into bloodstream in atrum in G cell, which acts back on parietal cell

160

what does ECL cell produce

histamine

161

what does Ach bind to in stomach (2)

1. parietal cells
2. ECL cells

162

what substances are involved in relaxation of stomach

Ach
NO
VIP
CCK

163

what substances trigger parietal cells to be activated

Ach
Histamine
Gastrin

164

alkaline tide

every proton pumped into lumen means a bicarb into bloodstream

165

which empties faster, carbs or fat

carbs

166

ileal brake

fat in ileum causes relaxation in stomach - slows down

167

gastrocolic reflex

induces need to defecate shortly after meal

168

gastroileal reflex

allows ileocecal valve to relax in response to gastric distention

169

what stimulates pancreatic secretion

Ach
CCK (stim by prot/fat)
Secretin (stim by acid)

170

what substances regulate ileal brake? (2)

peptide YY
GLP-1

171

what is the jejunum responsible for *2)

net absorption of bicarb and water

172

what is the ileum responsible for (3)

net absorption of NaCl, vitamin B12 and bile salts

173

what stimulates secretin secretion

-H+ in duodenum
- fatty acids

174

what does secretin do (4)

stimulates pancreatic secretion of bicarb

increases intestinal secretion of mucus and bicarb

increases hepatic secretion of bicarb and bile

inhibits gastric sercretion of acid

175

what stimulates CKK (2)

- fatty acids
- amino acids

176

what does CKK do (4)

increase pancreatic secretions

stims gallbladder to contract, relaxes sphincter of Oddi

inhibits gastric emptying

can potentiate the effect of secretin

177

Ach relationship with CKK and secretin

augments effects

178

when is GIP secreted

in response to all three types of nutrients

179

what cells secrete GIP

K cells in duodenum and jejunum

180

what does GIP cause (2)

stimulates insulin secretion from beta cells of pancreas

inhibits gastric hydrogen ion secretion

181

Hirschsprung's disease

congenital absence of myenteric plexus in distal portion of colon leading to functional obstruction and toxic megacolon

182

ghrelin secreted in response to what (2)

starvation
weight loss

183

leptin is secreted from where

adipose tissue

184

what does leptin do

inhibits ghrelin

185

peptide YY and CCK do what from where

in intestines, decrease appetite in response to nutrients

186

where are carbs absorbed

proximal - duodenum and jejunum

187

where are fats and proteins absorbed

all small intestine

188

where are bile salts and vit B12 absorbed

terminal ileum

189

where are iron and calcium absorbed

duodenum

190

what cells secrete CCK

I cells

191

what cells secrete secretin

S cells

192

what part of the pancreas does CCK work on

acinar cells to secrete enzymes (colipase, lipase etc.)

193

what part of the pancreas does secetin work on

ductal cells to secrete acqueous secretions like sodiumand bicarb

194

what kind of saccharides (poly, di, mono) are absorbed

mono only (glucose, galactose and fructose)

195

what parts of GI tract are resonsible for starch digestion

salivary glands (10-20%)

pancreas (80-90%)

small intestinal brush border (can break up di and trisaccharides)

196

sucrose is broken down by what into what

sucrase breaks sucrose down into glucose and fructose

197

lactose is broken down by what into what

lactase breaks lactose down into glucose and galactose

198

what transporter does fructose use to get from lumen to intestinal cell

GLUT5

199

what transporter does glucose, galactose and fructose all use to get from intestinal cell to blood

GLUT2

200

what transporter does glucose and galactose use to get from lumen into intestinal cell

SGLT1

201

what kinds of peptides can we absorb (amino acides, dipeptides, tripeptides, macromolecules etc.)

can absorb di, tri and amino acids (nothing larger)

HOWEVER, once inside the intestinal cell, di and tri peptides have to be broken down into amino acids in order to get into the blood

202

what protein cleaving enzymes exist in small intestine (4)

trypsin
chymotrypsin
carboxypepdidases (A and B)
elastase

203

what enzyme cleaves trypsinogen into trypsin

enterokinase

204

what does trypsin do

activates all the other enzymes (chymotrypsin, elastase, carboxypepditases A and B)

205

what kind of transporters do di and tri peptides use to get into intestinal cells

hydrogen ion dependent co transporters

206

what kind of transporters do amino acides use to get into intestinal cells

sodium dependent co transporters

207

CCK and gall bladder relationship

as a hormone CCK is stimulus for gallbladder to release bile

as a neurotransmitter, CCK feeds up to dorsal vagal complex to release Ach on gall bladder to also cause smooth muscle contraction

208

what kind of transporter is used to reabsorb bile salts from ileum back to liver

bile salt/ sodium cotransporter

209

What are the primary bile acids (2)

cholic acid
chenodeoxycholic acid

210

what is the rate limiting step in bile acid formation

the 7-alpha-hydroxylation of cholesterol

211

what happens to primary bile acids in colon

get dehydroxylated into secondary bile acids - deoxycholic acid and lithocholic acid

212

what happens to bile acids in liver

get conjugated to amino acids - glycine or taurine

213

what does colipase do

associates with micelle on fat droplet and attracts lipase so it can do its job (Without colipase the lipase would get kicked off fat droplet)

214

once in liver cell, what do these lipid components do

form chylomicron which then goes into lymph

215

cimetidine mechanism

H2 histamine receptor antagonists - directly block histamine-stimulated gastric acid secretion on parietal cells

specific and reversible

216

cimetidine adverse effects

least potent
renal elimination
can develop tolerance
crosses placenta

DRUG DRUG RXNS - inhibits a whole lot of p450 (warfarin too high etc.)

HORMONAL effects at high doses - increases prolactin, inhibits estradiol metabolism inhibits dihydrotestosterone receptor binding -- causes gynecomastia and impotence in lames and female galactorrhea

217

famotidine mechanism

(pepcid)
most potent
DECREASES % of ulcers in NSAID use

H2 histamine receptor antagonists - directly block histamine-stimulated gastric acid secretion on parietal cells

specific and reversible

218

famotidine adverse effects

renal elimination
can develop tolerance

219

sucralfate mechanism

mucosal protective agent - forms a paste at low pH that adhere to charged proteins of epithelial cells and ULCERS

take BEFORE meal

220

sucralfate adverse effects

can adsorb other drugs

don't coadmin with antaacids

221

bismuth subsalicylate mechanism

mucosal protective agent - active ingredient in pepto-bismol

forms bismuth oxychloride and salicylic acid in acid, binds selectively to ULCERS

is ANTIMICROBIAL

222

bismuth subsalicylate adverse effects

blackens stool and tongue

causes Reyes syndrome in chidlren

223

misoprostol mechanism

mucosal protective agent - prostaglandin analog (PGE1)

inhibits acid secretion from ECL and pareital cell

augments MUCUS and bicab secretion

224

misoprostol adverse effects

causes uterine contractions - CONTRA IN PREG

225

metoclopramide mechanism

anti-emetic
CENTRAL dopamine receptor antagonist

PERIPHERAL seratonin receptor agonist

can enhance ACh release in myenteric plexus, improves SM response to Ach

works against cytotoxic drug induced emesis

226

metoclopramide adverse effects

can cause parkinsonian like muscle spasms

227

ondansetron mechanism

selective seratonin receptor antagonist

works against cytotoxic drug induced emesis

228

ondanetron adverse effects

constipation

229

omeprazole mechanism

irreversible parietal cell proton pump inhibitor

is a prodrug - doesn't work unti lit gets to stomach

gets stuck in canaliculus in parietal cell

230

omeprazole adverse effects

crosses placenta
liver metabolized

slight risk of fractures and decreased B12 absorption

231

what is the first choice drug for zollinger ellison

proton pump inhibitors

232

antacin mechanism

weak base, neutralize stomach acid

233

Mg(OH2) adverse

diarrhea

234

Al(OH2) adverse

constipation

235

antacid drug interactions

many drug interactions because drugs depend on pH

alters urinary pH - traps acidic drugs

236

lubiprostone mechanism

chloride channel activator - increases intestinal fluid seretion via chloride mobilization

237

lubiprostone adverse effects

diarrhea, nausea

238

laxative vs carthartic effect

laxative - evacuation of soft stool from rectum

cathartic - increased intestinal activy and watery stool - ie for colonoscopy prep

239

linaclotide mechanism

chlroide channel activator - cystic fibrosis channel - increases fuild secretion

240

linaclotide adverse

diarrhea

contra in children

241

Mg(OH)2 mechasnism as laxative

osmotic laxative - osmotic presure leads to accumultion of fluids in gI tract and stimulation of perstalsis - works within 3 hours for colonoscopy prep

242

Mg(OH)2 laxative adverse

can cause hypermagnesemia in patients with renal insufficiency

243

loperamide mechanism

opioid - poorly absorbed, slow intestinal transit time -- antidiarrheal

244

loperamide adverse

constipation
risk of toxic megacolon in patients with UC or dysentery

245

IBS description

functional disease - no underlying structural abnormalities, no drug targets

246

alosteron use/mechanism

for women with diarrheal IBS you can use ALOSETRON which is a seratonin receptor antagonist

247

alosteron side effect

ischemic colitis

248

treatments for IBD

prednisone - anti-inflammatory, not useful for long term therapy

immunosupprssives - azathioprine, adverse is bone marrow suppression

249

azathioprine mechanism and enzymes that are present

anti-metabolite - gets incorporated into DNA/RNA

HGPRT needs to work to convert to active

TPMT can make it toxic to liver

XO makes it inactive

250

first line treatment for UC

mesalamines - sulfasalazine

251

sulfasalazine mechanism

obscure, but needs to be topical not systemic

252

sulfasalazine adverse

40% can't tolerate because of headaches, hypersensitivity, diarrhea, nausea, bone marrow suppression

253

infliximab mechanism and use

remicade
anti TNF-alpha
IV administered

254

adalimumab mechanism and use

humera
anti TNF-alpha
subcutaneous administration
100% humanized

255

infectious sialadenitis

infectious salivary gland disease caused by staph strep viridans and mumps

256

autoimmune sialadenitis

sjogrens - lymphocytic infiltrates destroy secretory cells - get dry mouth and dry eyes

don't see acinar structures, just glands - ducts

257

what is the most common benign salivary gland neoplasm

pleomorphic adenoma - frequencly recurs - more common than malignant

258

what is the most common malignant salivary gland neoplasm

mucoepidermoid carcinoma

259

major vs minor salivary neoplasms

major is more common and more commonly benign

minor is less common and more commonly malignant

260

pleomorphic adenoma characteristics (gross and histo)

encapsulated, freely movable, adpiose - white/tan
NO ULCERATION of skin

in histo - gross pattern is pleomorphic - very variable in appearance (have epithelial and myoepithelial cells, as well as stromal component)

261

mucoepidermoid carcinoma characteristics (gross and histo)

low grade and high grade (pain and speed of growth)

gross: unencapsulated, infiltrating, solid white pink, not well delineated

histo:
3 cell types - not a lot of stroma. epidermoid, intermediate and mucous cells - more mucous means lower grade

262

atresia

no functional lumen - developmental disorder between trachea and esophagus

263

achalasia

spasm of lES with esophageal dilation - commonly idiopathic but also can be due to Chagas disease

264

schatzki's ring/ web

LES ring = circumfrential

web = partial circumference in the upper esophagus

associated iwth iron deficiency (Plummer-Vinson syndrome)

265

Zenker's diverticula

upper - pulsion through weakened muscle

266

traction diverticula

adhesed to outside tissue - lower/middle of esophagus

267

esophageal varices

caused by cirrhosis or portal htn - most common cause of upper GI bleeding

268

Mallory Weiss syndrome

longitudinal linear laceration of small vessels at gastroesophageal junction - history of severe committing, most commonly seen in alcoholics

269

esophagitis causes (3)

infection - viral: herpes, CMV, fungi: candida, bacterial superinfection

chemical - drugs, lye

reflux of gastric juice - peptic esophagitis leading to ulceration and epithelial metaplasia

270

Barrett Esophagus

metaplasia to columnar epthelial will GOBLET CELLS (looks intestinal) that replaces squamous epithelium

271

esophageal cancer types

adenocarcinoma (most common in US) - from Barret's, at GE junction - histo has glands and goblet


squamous cell (most common world-wide) - mid-low esophagus. histo looks like swirls

272

what is in oxyntic mucosa and where is it

fundus and body - has cheif cells and pareital cells

273

causes of pyloric stenosis

congenital and aquired (complication of PUD)

274

Menetrier's disease

hypertrophic gastropathy - ideopathic incrased TGFalpha induced hypertrophy of mucous cells and rugae - atrophy of parietal cells

275

gastritis - causes

H. Pylori, NSAIDS, Cig, alcohol, gastric hyperaciditiy, duodenal-gastric reflux

ischemia, shock, delayed gastric epmtying

276

what inflammatory cell type do you see in acute gastritis

neotrphils in lamina propria

277

erosion vs ulceration

erosion is mucosa only, ulceration extends through submucosa

278

what inflammatory cell types do you see in chronic gastritis

lymphocytic infiltrate - and plasma cells etc.

undergoes metaplasia

279

autoimmune metplastic atrophic gastritis - location and associated disorders

in body-fundus
attacks parietal cells - diecreased acid production

associated with pernicious anemia

and neorendocrine tumor

280

H pylori gastritis - location and associated disorders

in antrum - swims in mucous layer and secretes urease - increases acidity

association with peptic ulcers

and lymphoma (MALToma)

281

levels of gastric ulcers (4)

1. superficial necroinflammatory debris with necrosis and neutrophils

2. acute inflammation - polys (neutrophis)

3. chronic inflmmation (lymphocytes) and granulation tissue

4. fibrosis scarring

282

gastric polyp types

epithelial cell growth - benign

1. inflammatory - most common
2. adenomatous - low grade dysplasia - associated iwth chronic gastritis
3. hamartomatous

283

benign UGI tumors (2)

leiomyoma - more common - SM

schwannoma - peripheral nerve tumor

284

malignant UGI tumors (3)

adenocarcinoma - associated iwth chronic gastritis - associated with asians, metastesizes. intestinal and infiltrative types

lymphoma - associated with chronic gastritis H.Pylori

gastrointestinal stromal tumor

285

signet ring seen with what cancer

infiltrative adenocarciona type

286

gastrointestinal stromal tumor - identification and tx

CD 117 positive
looks like spindle cells in histo with mitoses

tx with gleevec

287

Gastroperesis definition

impaired transit of contents from stomach to duodenum

288

types of gastroperesis (2)

1. neuropathic
2. myopathic

289

extrinsic innervatino os stomach

vagal (para)
splancnic (symp)

290

intrinsic innervation of stomach

1. interstitial cells of Cajal
2. enteric nervous system

291

pacesetter rate of stomach

3 contractions per minute

292

what neurotrasmitters/hormones help with accommodation

VIP and NO -- via vaso-vagal reflex

293

neuromuscular causes of gastroparesis (4)

1. DM
2. parkinson's
3. scleroderma
4. duchenne's muscular dystrophy

294

infiltrative causes of gastroparesis (2)

1. malignancy
2. amyloid

295

infectious causes of gastroperesis (4)

1. herpes zoster
2. lyme
3. trypanosoma cruzi
4. EBV

296

medication causes of gastroparesis (3)

1. anticholinergics
2. opiates
3. L-Dopa

297

metabolic causes of gastroparesis (3)

1. hyperglycemia
2. renal insufficiency
3. hypo/hyper thyroid and parathyroidism

298

gastric emptying study

use technitium sulfur - measure at 1, 2, and 4 hours for delayed emptying

299

gastroparesis diet

low fat, low fiber, 6 small meals per day

300

gastroparessis pharmacology tx (4)

prokinetics - metoclopramide, erythromycin, domperidone (no BBB)

anti-emetics

antidepressants

pyloric botox injection

301

how do NSAIDS cause PUD (2)

1. direct corrosive damage
2. systemic inhibition of prostaglandins (main driving force of damage)

302

coadmin of what drugs with NSAIDS increase risk of PUD (2)

1. corticosteroids
2. anticoags

303

when do you take PPIs

30-40 minutes before a meal

304

first line tx for H. pylori (3)

1. PPI
2. clarithromycin
3. amoxicillin or flagyl

305

risk factors for stress ulcers (3)

1. mechanical ventillation
2. coagulopathy
3. burns


all cause reduced mesenteric perfusion

306

marginal ulcer cause

roux en Y bypass within 6 months after surgery
- ischemia

307

diagnostic tests for H pylori (3)

1. stool antigen test

2. urea breath test

3. serum IgG antibody - high false positive (low specificity)

308

when should you retest for H Pylori

4 weeks after tx to rule out false pos and false neg

also because resistance is increasing

309

why repeat endoscopy after H pylori tx - and when

to see if there's still an ulcer - indicates cancer - 8 weeks after

310

dimensions of esophagus

20cm long, 2cm diameter

311

does esophagus of adventitia or serosa

adventitia

312

two types of dysphagia (2)

oropharyngeal
esophageal

313

type A ring

muscular

314

type B ring

diaphragm like (shotzki's) -

315

corkscrew esophagus

esophageal spasm - manometry dx tool

316

tx for esophageal spasm (3)

calciumc channel blockers, nitrates

botox

myotomy (last case)

317

achalasia dx requirements (2)

1. incomplete relaxation lf LES
2. abnormal motility on manometry

318

treatment for achalaisa (3)

1. myotomy - disrupt LES
2. botox
3. calcium channel blocker

319

angle of HIS

prevents reflux of stomach contents into esophagus

320

4 mechanisms of reflux

1. transient lower esophageal sphincter relaxations (tLESR)

2. swallow induced LES relaxations

3. hypotesnsive LES pressure

4. hiatal hernia and the "acid pocket"

321

complications of GERD (4)

1. upper GI bleed
2. benign peptic stricture
3. barrett esophagus
4. esophageal adenocarcinoma

322

surgery for GERD

nissen fundoplication - tighten sphinchter - wrap stomach around

323

which is more common, GERD or NERD

NERD

324

treatment plan for GERD

dietary changes

if persists, then PPI or H2 antagonist

if persists, upper endoscopy

325

specialized lymphocytes in GI tract (2)

IEL
MAIT cells

326

what are M cells

cells in epithelium of GI tract that uptake antigen and transport to tissue of gut

327

what antibody do plasma cells in gut produce predominately

IgA

328

small vs large intestine - whcih has more microbes and mucus

large has more of both

329

Th17 and the gut

promotes barrier function - tight junctions, defensin production etc.

330

mucous and IgA

mucin interactions with glycoproteins in mucous, which stabilizes IgA and reduces turnover (same with IgM too - lesser extent)

331

how does IgA get from plasma cell to lumen

gets transcytosed - associated with "Secretory component" from poly-Ig receptor

332

sequence of events to make effector T cell (4)

1. dendritic cell processes antigen, presents it with MCH class 1 or 2

2. costimulation with T cell in peyers patch - cytokines hat stimulate T cell differentiation and activation

3. T cells help B cells to make cytokines that isotype switch and differentiation into plasma cell

4. goes out through lymph and hones back through chemoattraction to go back to GI epithelium

333

when do we get colonized with bacteria

at birth (vaginal canal)
and boost at 3-6 months with food intake

334

c. diff microbiome treatment

stool trasnplant

335

childhood pancreatic islet autoimmunity microbiome tx

earl yadmin of probiotic supplementation

336

TGF-beta and inflammatory response (2)

stimulates differentiation of T-reg cells (through IL-10) decrease proinflammatory responses

TFGb also regulates B cells to switch to produce IgA

337

IL12 and inflammatory response

promotes differentiation of T cells into Th1 and Th17 - pro-inflammatory

(also by IL-17, 22, IFN-g and TNF-a)

338

antibiotics and microbiome effects (4)

1. decreases diversity of gut flora
2. decreases mucous layer
3. decreased efficacy of PD-1 blockade in tumor suppression
4. obesity phenotype transplantation - food metabolism

339

microbiome, inflammation and plant-based diet

plant-based increases production of short chain fatty acids which increase production of Treg cells and create anti-inflammatory environment

340

why is IgA deficiency often asymptomatic

body still makes IgM and is host-protective

341

jejunal gross/histo structures (3)

1. submucosal plicae circularis
2. long villi with branched and expanded tips and internal lacteals (holes) and crypts of libercuhn
3. tall columnar absorptive cells with interspersed goblet cells

342

ileum gross/histo structures (2)

1. lots of submucosal lymph nodules
2. villi are blunter, crypts of libercuhn

343

vermiform appendix structure (2)

1. all layers of regular gut tube, but has PITS, no villi
2. lots of lymphoid tissue

344

colon histo/gross structures (4)

1. mucosa is pitted and folded (NO VILLI)
2. numerous goblet cells, tall columnar absorptive cells
3. periodic thick external outer long muscle - taenia coli
4. posterior ascending and descending have adventitia -- secondarily retroperitoneal

345

colon function

1. home to microbiome
2. water absorption

346

rectoanal junction structure (4)

1. muscularis mucosae ends abruptly at pectinate line
2. colonic mucosa to stratified squamous un- to keratenized
3. venous plexuses - hemoroidal
4. lymph tissue

347

assmiliation

= combo of absorption and digestion

348

how much fluid is absorbed per day in GI tract

8-10L

349

ions that drive absorbtion and secretion

absorption (of water, nutrients, electrolytes, bile salts) in villi driven by sodium absorption via solvent drag

secretion in crypts driven by Cl secretion (disregulation causes diarrhea)

350

absorption of what happens where along small intestine

nutrients in proximal SI

electrolyte transport in distal SI

bile salt absorption in terminal ileum

all coupled with sodium driven by gradient established by Na/L ATPase

351

transporters in different parts of colon

in right colon - sodium uptake happens via Na+/H+ exchange

in left colon - sodium uptake occurs via ENaC (aldosterone sensitive) channel and K+ secretion occurs simultaneously

352

jejunum and duodenum - what amount of fluid is absorbed

5L - high volume, low efficiency

353

what channels regulate secretion in GI tract

3 chloride channels - CIC-2, CFTR, CaCC

354

how does CFTR channel get opened (2)

1. VIP --> Gs protein --> cAMP --> protein kinase C phosphorylates CFTR and opens channel

2. cGMP --> different protein kinase which phosphorylates CFTR and opens channel

355

cholera mechanism

1. cholera toxin binds to G protein permanently activating, keeping channel open and pumping chloride ion out

2. cholera toxin also binds Na+/H+ exchanger causing decrease in sodium uptake (decreased absorption ability) -- give glucose to oral rehydration therapy which will drag sodium in with it

356

what stimulates calcium activated chloride channel (2)

Ach (increases calcium)

ecoli increases intracelluar calcium also

357

volume definition of diarrhea

an increase in stool fluid volume of more than 200mL within 24 hours

358

malabsorpbtion causes what kind of diarrhea

osmotic diarrhea

359

toxins (like cholera) cause what kind of diarrhea

secretory diarrhea

360

diarrhea causes what to potassium and pH levels

causes loss of K+ and bicarb - so you get hypokalemia and metabolic acidosis

361

what to give someone with cholera to maintain fluid levels

- give glucose to oral rehydration therapy which will drag sodium in with it

362

where does calcium absorption happen, what's it stimulated by

duodenum - stimulated by calcitriol from vitamin D

363

bacterial enzymes help metabolize what (2)

bile acids
fiber

364

dietary fiber digestion

amylase can't break down nonstarch polysaccharides

bacterial fermentation causes breakdown into short-chain fatty acids (which in turn pH keeps bacterial overgrowth in check)

365

rectal distension and anal sphincters

rectal distension causes relaxation of internal sphincter and excitation of external sphincter, and then we have voluntary control over relaxing external sphincter

366

Knudson's 2 hit hyptohesis

what is needed to develop cancer - cancer needs to same mutation of tumor suppressor gene on both allele

367

on average how long does it take for adenoma to get to cancer

10-15 years

368

familial adenomatous polyposis (FAP)

80% inherited autosomal dominant germiline mutation in one allele in APC tumor suppressor gene on chrom 5 - second allele mutation during childhood - ton of polyps by age 16, screen at age 10

369

lynch syndrome

mismatchrepair gene autosomal dominant - 2-4% of colon cancers

also presents with endometrial cancer

370

when to resect liver with colon mets

at least 20% functional liver needs to remain

ensure at least 1mm margin

371

4 serious sequelae of enteritis

1. hemolytic uremic syndrome (HUS) due to shiga producing E. Coli

2. Guillain-Barre syndrome (GBS) caused by campylobacter

3. IBS

4. chronic malnutrition and increased susceptibility to other diseases (malaria, TB)

372

what kind of bacteria cause infectious enteritis (gram staining, shape etc)

gram neg rods

373

major bacterial culprits (8)

1. salmonella
2. capylobacter
3. shigella
4. E coli
5. clostridium dificile
6. vibrio
7. yersinia
8. listeria (extremes of age)

374

what kind of diarrhea is associated iwth entero vs cytotoxins

cytotoxins have bloody diarrhea

375

examples of enterotoxins (2)

1. cholera toxin
2. E coli heat labile and stable toxins

376

examples of cytotoxins (2)

1. shiga toxin (from E. Coli and shigella)
2. c diff toxin B

377

examples of neurotoxins (3)

preformed in food - cause immediate vomitting (enterotoxin later causes watery diarrhea)

1. staph aureus
2. B cereus
3. clostridium botulinum

378

what kind of diarrhea do viruses cause

secretory - watery

379

vibrio cholera - transmission, clinical, management

comma-shaped

1. foodborne/ waterborne
2. abrupt onset of massive rice water stool
3. oral rehydration with glucose, antibiotics

380

ETEC - transmission, clinical, management

1. food and water - uncooked veggies, unpeeled fruit, uncooked meat etc.

2. main cause of traveller's watery diarrhea

3. antibiotics and/or antimotility agents (but immunocompetent will recover okay)

381

what is dysentery

bloody diarrhea and fever

382

site of intestinal action for secretory vs inflammatory diarrhea

secretory = small intestine

inflammatory = colon

383

shigella - characteristics, transmission, clinical, treatment

shigella does NOT have H antigen - no flagella, shigatoxin has AB5 structure

1. fecal-oral, food and water

2. fever, cramps, watery to bloody diarrhea, high mortality. can progress to HUS and reactive arthritis

3. tx with fluoroquinolones

384

capylobacter - characteristics, transmission, clinical, treatment

1. comma shaped gram neg rod

2. transmission - zoonotic, poultry (jejuni) cattle/sheep (fetus)

3. jejuni causes enterocolitis, fetu causes sstemic disease. associated with GUILLAIN-BARRE, reactive arthritis, septic abortion

4. tx fluoroquinolones

385

STEC - characteristics, transmission, clinical, tx

1. E coli O157:H7 - hamburger disease

2. food borne (meat, soy butter), water borne, swimming pools

3. non-bloody within hours, bloody within 1-2 days, HUS concern - renal involvement

4. supportive management - NO ANTIBIOTICS - will increase chances of HUS

386

non-typhoid salmonella - characteristics, clinical, tx

1. different serovars

2. foodborne - eggs, poultry etc and contact wit REPTILES

3. bloody diarrhea, extra-intestinal seeding in bones/joints (esp sickle cell) and endovascular

4. might have to remove gall bladder (CHRONIC CARRIAGE)
tx for immunosuppresssesd or heart valves - fluoroquinolones

387

typhoid salmonella - symptoms, dx, tx

AKA enteric fever - don't focus on GI symptoms

gets into blood stream - prolonged fever and bacteremia. see ROSE SPOTS salmon maculopapular rash and HEPATOSPLENOMEGALY
high mortality if untreated - intestinal perforation, endocarditis

blood culture, bone marrow, tx with fluoroquinolones, can have chronic carriage - source of secondary infections (typhoid mary)

388

what pathogens cause chronic diarrhea

PROTOZOA - not virus or bacteria

389

giardia - transmission, symptoms, diagnosis

water transmission - camping

foul-smelling stool, fat malabsorption, no blood in stool

dx by seeing cysts on smear and fecal antigen test PCR

390

cryptosporidium - smptoms and dx

acid fast smear

watery chronic diarrhea in HIV pos, need to get CD4 up

391

cyclospora - symptoms dx

acidd fast staining of feces

lots of gas, explosive diarrhea, fatiue

foodborne outbreaks

392

amoebiasis clinical, dx

two phases - dysenery (with flask ulceration) and liver abscess

stool PCR and antigen testing but can have negative stool microscopy if only in liver

393

when to do diagnostic test with diarrhea

dysentery, sepsis, suspected outbreak, food-handler, c. diff

394

when do you give antimotility agents like loperamide/imodium

only when there's watery diarrhea - don't give with bloody diarrhea, don't want to prolong the organisms' s stay in the gut

395

when to give antibiotics for diarrhea (5)

1. severe/persistant diarrhea

2. enteric fever

3. traveler's diarreah

4. c. diff (metro, oral vanc)

5. giardia, E. histolytica (metronidazole)


NOT STEC - WILL GIVE YOU HUS

396

secretory diarrhea definition

continues despite fasting, more than a liter

397

osmotic diarrhea definition

ceases with fasting, less volume than secretory

398

formula for stool osmotic gap and criteria for high and low

290 - 2(stool Na + stool K)

greater than 125 mOsm/kg suggests osmotic diarrhea - large quant of unmeasured non-electrolytes magnesium, phosphate, lactose intolerance

less than 50 is secretory - incomplete absorption of electorlytes - cholera

399

what do lactoferrin and calprotectin indicate

inflammatory diarhea

400

choleretic diarrhea cause and tx

ileal resection LESS THAN 100cm, malabsoprtion of bile acids, bile acids stimulate choride and fluid secretion in colon causing choleretic diarrhea

tx with cholestyramimne, a ibile acid binding resin

401

fatty acid diarrhea cause and tx

ileal ressection MORE THAN 100cm, bile acid malabsorption results in delivery to colon, hepatic synth can't catch up, bile acid pool is depleted

WORSENS with cholestyramine

402

oxalate kidney stones and malabsorption

fat malabsorption (short bowel for example) oxalate gets into colon and gets sent to kidneys where they form stones

403

how to test for lactose intolerance

bacteria produce H2 when it hits malabsoprtbed carbohydrate

404

how to test for SIBO

give lactulose, measure peak of H2 breath hydrogen testing

405

direct vs indirect inguinal hernia

indirect follows path of scrotom through inguinal ring.

direct is through weakening of abdominal wall

406

pathological findings in abetalipoproteinemia

inherited autosomal recessive absense of apoprotein fails to mobilize Lipids into circulation - see LIPID VACULOES in enterocytes, RBC "BURR CELLS" and demyelination in the CNS

407

what do you see in pathology of section of dermatatis herpetiformis, and what is it associated iwth

celiac

see subepidermal vesicles filled iwth neutrophils

408

whipples disease - cause, symptoms, histo

caused by tropheryma whipplei bacteria

affects middle aged men, get fever, migratory arthritis and diarrhea

in histo see foamy macrophages with PAS+ rod like bacteria, and flattening of villi

409

peutz-Jegher polylps - associations

hamartomatous - inherited autosomal dominant, associated iwth mucosal pigmentation and non-GI cancer

410

Juvenile popylposis - associations

autosomal D, large polyps, associated iwth GI cancer

411

do hyperplastic polyps have stalks?

usually no

412

do tubular adenomas have a stalk?

usually yes

413

do villous adenomas have a stalk

no - they're sessile

414

do tubulovillous adenomas have a stalk?

usually yes

415

what do hyperplastic polyps look lik eon histo

frilly serrated appearance that stop HALF WAY down crpt. crypt base is narrow

416

sessile serrated polyp look like on histo

serrated epithelium extends all the way down, usually in right colon, base of crypts are dilated, higher risk of BRAF microstellite cancer

417

carcinoid syndrome

caused by neuroendocrine tumor - causes excess serotonin production leading to sporadic hypertension, asthma, diarrhea and flushing -- due to liver mets

418

IBD specific serology (3)

ASCA - cerevisiae - higher in crohns disease

DNase sensitive pANCA - histone H1 - higher in UC

OmpC - E coli - higher in CD

419

central arthritis associated with IBD

ankylosing spondylitis (independent of disease process) associated with UC

420

peripheral arhtritis associated iwth IBD

runs parallel to disease course of UC - monoarticular, migrating, joint pain

421

skin associations iwth UC

1. erythema nodosum
2. pyoderma gangrenosum

422

what do you use 5-ASA drugs for

UC

423

Ogilvie's

pseudoobstruction and mild pain - caused by drugs, surgery, neurological problem