Exam 1 Flashcards
(423 cards)
1
Q
does esophagus have serosa?
A
upper esophagus = no serosa
lower esophagus = serosa (intraperitoneal)
2
Q
oral mucosa histological characteristics/layers
A
- stratefied squamous unkeratinized/lightly keratinized epithelium
- underlying CT - lamina propria with BVs
3
Q
saliva contents (4)
A
- secretory IgAs
- beta defensins from epithelial cells (antibacterial)
- amylases
- lysosyme
4
Q
tongue histology features (5)
A
- strategied squamous unkeratinized/slightly keratinized
- 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)
- lots of skeletal muscle (intrinsic and extrinsic)
- minor salivary glands (mixed or either or, associated with folate and circumvalate)
- lingual lymph nodes (GALT)
5
Q
difference between the nuclei of supportive and sensory cells in taste buds
A
sensory have rounder, lighter stained nuclei,
supportive have darker and more elongated nuclei
6
Q
what tastes can you detect
A
sugar salt bitter sour umami
7
Q
are sensory cells attached to myelnated or unmyelinated nerve fibers
A
myelinated
8
Q
minor salivary glands are where
A
all over oral cavity
9
Q
what are major salivary glands (what are they made of)
A
- parotid (mostly serous - amylase, proteinaceous)
- submandibular (mix of serous and mucous)
- sublingual (mostly mucous acini)
10
Q
mucous vs serous characteristics
A
mucous is lighter than serous
11
Q
ducts
A
intercalated to striated to interlobular and main excretory
12
Q
what makes enamel
A
ameloblasts
13
Q
what is deep to enamel
A
dentil, which is vital, innervated, and bone-like
14
Q
what secretes dentin
A
odontoblasts. odontoblasts processes radiate throughout dentin in dentinal tubules, like osteocyte processes in canaliculi of bone
15
Q
how many teeth to children have
A
20 primary teeth
16
Q
which teeth are lost first to last
A
- central incisors
- lateral incisors
- first molar
- canine
- second molars
17
Q
how many teeth do adult have
A
32
18
Q
tooth development stages
A
- ectoderm thickens as dental lamina
2. invaginates due to inducement of NCC mesenchyme called dental pipilla
19
Q
what do NCC develop in teeth
A
odontoblasts (dentin) and pulp of tooth
20
Q
what does ectoderm form in teeth
A
ameloblasts (enamel)
21
Q
oropharynx histologic characteristics (4)
A
- SS uK epithelium
- lamina propria
- submucosa with lymphoid follicles
- skeletal muscle in walls
22
Q
how long is the human GI tract
A
30 feet
23
Q
myenteric is associated with what layer
A
muscular
24
Q
auerbach is associated iwth what layer
A
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
