GI Pathophysio Flashcards

1
Q

vitamin a deficiency

A

night blindness

bitot spos (squamous cell prolif)

corneal perforation

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2
Q

How to diagnose diverticulitis

A

clinical if mild

CT scan or ultrasound

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3
Q

epithelium of the stomach

A

simple layer of columnar epithelial cells

secrete mucus and bicarb

pits provide glands access to the lumen

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4
Q

symptoms of pancreatic exocrine insufficeincy

A

bulky foul smelling stool

oily residue in toilet water

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5
Q

irritant laxatives

A

castor oil, senna

cause irritation of the enteric mucosa/nerves –> water secretion –> softer stool and increased peristalsis due to increased volume

may cause abdominal pain, flatulents

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6
Q

bile acid deficiency

A

when bile salt pool is very low, get maldigestion of fat and fat soluble vitamins

from liver disease (low production) or ileal resection (low recycling)

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7
Q

trituration

A

first, peristalsis down through stomach

terminal antral contraction closes pyloris

allows mixing of foodstuff into small particles until 1-2 mm

3-4 hours

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8
Q

NSAIDs and ulcer formation

A

decrease mucin and HCO3 so HCl can touch the cell

injury to cell - HCl can get closer!

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9
Q

vitamin D

A

fat solumble

storage form = 25OH, active form 1, 25 OH

found naturally in very few foods (fortified and sun)

calcium-phosphorus homeostasis (break down bone if not enough)

bone metabolism

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10
Q

IBS

A

Rome criteria -

absence of detectable structural or biochemical abnormaility

abdominal pain

altered bowel habits (alternating between diarrhea and constimation)

abdominal pain is most universal!

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11
Q

IBS-C

A

IBS with constipation

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12
Q

how do you diagnose celiac disease?

A

high antibody levels to: TTG IgA, DPG (deaminated peptide)

abnormal small bowel biopsies

response to gluten free diet

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13
Q

consequences of bacterial overgrowth

A

unconjugate bile acids

use vit b12

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14
Q

treatment of pancreatic exocrine insufficiency

A

pancreatic enzyme supplements wiht food

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15
Q

viberzi

A

binds to opioid receptors in GI tract controling motility and hypersensitivity

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16
Q

types of glands in the cardia

A

branched and tortuous

mucus

endocrine

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17
Q

pancreatic exocrine insufficiency

A

maldigestion of fat, protein, carbs

limited amylase, lipase, proteases

from CF, chronic pancreatitis, pancreatic resection

need to lose >90%

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18
Q

pre-epithelial defense in the esophagus

A

lacks a definable surface mucus layer!

has saliva which contains mucins

surface squamous cells can not secrete bicarb! rel unprotected

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19
Q

esohageal peristalisis in smooth muscle

A

inhibition followed by excitation

gradient of increasing inhibition (latency gradient)

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20
Q

beri beri

A

B1 deficiency

dry - peripheral neruopathy

wet - CHF

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21
Q

vitamin d deficiency

A

bone demineralization

hypocalcemia, hypophosphatemia

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22
Q

B12 absorption

A

dietary intake (meat, dairy)

pepsin in the stomach cleaves protein from B12

secretion of IF by gastric parietal cells

bound to R protein

unbound - binds to IF in the intestine

in the ileum - special R and complex absorbed into blood

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23
Q

diverticular bleeding pathophysiology

A

eccentric intimal thickening and medial thinning

segmental weakening

rupture where vessels run over the dome of a diverticulum

usually abrupt and painless - 75% stops on own

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24
Q

erythromycin

A

primarily prokinetic

motilin receptor agonist

The main function of motilin is to increase the migrating myoelectric complex component of gastrointestinal motility and stimulate the production of pepsin. Motilin is also called “housekeeper of the gut” because it improves peristalsis in the small intestine and clears out the gut to prepare for the next meal.[7] A high level of motilin secreted between meals into the blood stimulates the contraction of the fundus and antrum and accelerates gastric emptying. It then contracts the gallbladder and increases the squeeze pressure of the lower esophageal sphincter. Other functions of motilin include increasing the release of pancreatic polypeptide and somatostatin[11]

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25
uncomplicated diverticulosis
asymptomatic - incidental, increase fiber symptomatic - bloating, constipation, passage of mucus, like IBS
26
bethanechol
prokinetic muscarinic receptor agonist
27
Cholestyeramine (questran)
bile acid sequentrant, prevent reabsorption bile acids, once complexed, are secreted in feces lower plasma cholesteral used to prevent diarrhea pst ileal resection
28
d-xylose test
for carb malabsorption ## Footnote D-xylose = simple sugar, some absorbed and some excreted If absorbed – some metabolized by liver and some excreted by kidney If not absorbing – none in blood stream and none in urine Fasting – empty bladder, blood draw Drink solution of sugar water – 2 hours later, repeat bloodd draw and see if blood level went up properly Collect urine over 5 hours and see if xylose is in there – if really low not absorbing properly and sign of absorption problem
29
sibship size and gastric cancer risk
higher risk of cancer in later bown higher risk with brothers and sisters early years of life affect health decades later
30
gastric motility of liquids
rapidly disperse through stomach and empty without delay
31
prokinetics
Prokinetics help strengthen the lower esophageal sphincter (LES) and cause the contents of the stomach to empty faster. more gerd? combined prokinetic/amtoe,etoc
32
mixed micelles
transport lipolytic products (mostly fA and MG) hydrophilic part on outside
33
vitamin K
dietary from plants, synthesize by gut bacteria essential to function of blood clotting factors
34
bulk laxatives
i.e. metamucil, citrucel absorb water, increase in stool volume triggers stretch receptors and causes reflex peristalsis that propels bowel contents forward safe, most physiologic fiber laxatives 12 hrs to tdays to work vegetable fibers
35
stimulant laxatives
derivatives of phenolphtalein induce high amplitude propagated colonic contracts appear to be safe! rescue agents when no BM for several days
36
37
opiates
systemic antidiarrheals slow peristalsis - allow increased water reabsorption
38
gastric motility of solids
lag phase then trituration rate depends on nutrient content too (fat is slowest)
39
fundoplication
surgical repair for hiatal hernia ## Footnote The important one is called a surgical fundoplication, where the stomach, the fundus of the stomach over here (black arrow) which was originally over here (lavender arrow) is wrapped around the LES and sort of adds to its pressure.
40
how to diagnose gastroparesis
EGD to r/o obstruction scintigraphy = gold standard
41
IBS pathophysiology
genetic/social factors + food and stress lead to symptoms
42
pseudoachalasia
malignancy (gastric) paraneoplastic chagas eosinophilic gastroenteritis infiltrative process at LES
43
tissue transglutaminase
deamidates or crosslinks gliadin - increasing its affinity for receptors on WBCs
44
folate
DNA synthesis
45
pathogenesis of diabetic gastroparesis
chronic hyperglycemia --\> neuropathic changes and dysfunctional innervation through the vagus --\> delayed gastric emptying due to autonomic neuropathy
46
Transient lower esophageal sphincter relaxations (TLESR)
occur primarily postprandially (facilitate belching) occur in healthy and GERD pts in the same amt propriton of reflux related to TLESR is greater in patients w GERD1 Well, what’s happening is all of a sudden in these sort of recordings, we see that in certain patients, they get these transient relaxations that are not associated with a a swallow (points at blue arrow segment) So the sphincter just relaxes on its own, it’s usually a very prolonged relaxation, and that if you noticed, can cause the esophageal acidity to go down for a long period of time after it’s already relaxed for awhile and the reflux bolus goes up, you try to swallow it back down, but even so you might get a prolonged exposure of the esophagus to acid.
47
48
Barrett's Esophagus
in response to acid reflux normal squamous epithelium may be replaced by columnar epithelium of the specialized intestine type ## Footnote 1% chance of adenocarcinoma (increasing!)
49
serotonin
imp NT and gut signaling molecule major modulator brain-gut communication activates enteric neurotransmission to initiate peristalsis and secretion
50
selenium deficiency
cardiomyopathy
51
vitamin E
anti-oxidant
52
short bowel with SHORT ileal resection
bile salt diarrhea bile acids are incompletely reabsorbed for circulation back to the liver bile acid spillage into the colon is irritating causing a secretory diarrhea Tx: bile acid resins
53
percent weight loss
(UBW - Actual BW)/UBW x 100
54
3 hypotheses of diverticuli
1. altered colonic wall structure: weak pts in the colon wall where the vasorecta penetrate from the muscularis propria into the submucosa 2. abnormal motility: normally pressures are equal through colon, but increased segmentation in diverticular colons --\> increased intraluminal pressures --\> predisposes to hernieation 3. dietary fiber: less risk with more fiber! fiber increases colon diameter, bulks stool, prevents increased P
55
hydrogen breath test
to test for lactase deficiency HBT – lactase maldigestion Fasting – blow into tube and blow baseline hydrogen methane production, drink lactos and blow into the tube every 20 min for a few hours If gas levels peak to certain pt – lactose is not digested and lactase is delivering a lot of gas If symptoms also – they are lactose intolerant –
56
short bowel syndrome
severe malabsorption condition following extensive small bowel resection post duodeal length less than 5 feet prone to severe diarrhea and weight loss due to rapid transit, lack of intestinal surface area, bile acid spillage, residual disease (crohns) causes: adults - intestinal ischemia, crohns volvulus trauma children -- congenital
57
niacin
B3
58
fundic accomodation
swallow initiation - fundus undergoes vagally mediated (NITROUS OXIDE!) relaxation - as meal enters the stomach, tnic and phasic contractions are inhibited - 2-3x increase in gastric volume!
59
h pylori and esophageal disease
60
vitamin e deficiency
hemolytic anemia neuro (ataxia, peripheral neuropathy, myopathy
61
if eye or vision problems?
vit A zinc 9f night blindness
62
Treatment for SIBO
antibiotics correct underlying cause
63
mucosal phase of digestion
brush border hydrolysis transport into epithelial cells (enterocytes) when abberent - malabsorption
64
reciporcal relationship between adenocarcinomas of stomach and esophagus
65
if oily scaling around nares?
riboflavin or zinc deficiency
66
treatment of IBS
mutlidiscplinary education and reassurance dietary (avoid exacerbations w lactose, low FODMAP diet) stress management meds
67
how to diagnose achalasia?
endoscopy (not swallowing) barium swallow manometry\*\* gold standard
68
gliadin
one of two types of protein that are components of gluten in wheat contains the toxic AA sequences
69
secretagoges
Amitzia latest laxatives stimulate net efflux of ions and water into the intestinal lumen accelerate transit and facilitate defectatin activates Cl channels on apical - Cl rich fluid secretion - softens stool, increases motility, promotes Pm
70
pantothenic acid
B5
71
HLA DQ2 and HLA DQ8
receptors on WBCs bind gliadin fragments and trigger an inflammatory cascade celiacs cytokines --\> more inflam cells --\> tissue damage \*\*during this process abs against TTG and deaminated gliadin develop
72
adherence pedistal
h pylori forms with epithelial cell to insert proteins ## Footnote Consistent with that is the fact that HP is very smart and understand human biology well * Slide shows epithelial cell and HP that have been cocultured * Epithelial cell has formed adherence pedestal [points to supporting structure at bottom of oval blob] * Helical cell has instructed the cell to form the pedestal through polymerization of actin
73
colonic diverticulosis
sac like protrusion of the colonic wall mucosa and submucosa herniate through the muscularis
74
intrinsic LES
smooth muscle gastric sling fibers So, remember the LES is sort of a complex apparatus It’s made up of intrinsic components, so we have the smooth muscle layers of the lower esophagus coming down so that’s the longitudinal and circular muscle layers. And then there’s also an extrinsic component which is primarily made up of diaphragm so when there is no hernia or no sort of anatomical defect, this diaphragm contributes to the tone of the LES.
75
symptoms of SIBO
gas/bloat diarrhea maybe B12 deficiency? Bacteria uses B12
76
treatment for lactase deficiency
limit lactose containing foods use lactase supplements
77
esophageal cancer and cancer
adenocarcinoma!
78
vitamin c deficiency - clinical manifestations
swollen bleeding gums loose teeth petechiae periungal hemorrhage impaired wound healing arthalgias, joint effusions corkscrew hair anemia
79
cause of achalasia
uncertain autoimmune? altered inhibitory innervation of smooth muscle loss of peristalsis failure of les relaxation
80
tricyclic antidepressents
IBS inhibitory effect on gut - alleviate symptoms at a very low dose \*amitripyline - take at sub depression levels
81
IBS-M
constipation and diarrhea
82
the bowel disorders
IBS functional diarrhea functional constipation
83
inhibitory innervation in the esophagus
more distal
84
how do you diagnose pancreatic exocrine insufficiency?
fecal elastase level - ## Footnote Stool test – elastase – if enough pancreatic enzymes are in bowel and going into stool Stool test to measure amt in the stool
85
86
types of glands in antrum
endocrine mucus g cells (gastrin)
87
impedence-pH monitoring
place transnasally for 24 hours can detect liquid, air, reflux adds impedence data - detection of changes in ersistance - detects all liquid reflux events from stomach to esophagus
88
area postrema
has chemoreceptor trigger zone (CTZ) sensitive to many stimuli
89
diverticulitis
likely due to increased lumenal pressure and thickened particulate matter that causes wall erosion, inflammation, perforation uncomplicated complicated - abcess, fistula, peritonitis (LLQ pain, nausea, fever)
90
cobalamin
B12
91
h pylori induces what kind of cancer?
adenocarcinoma
92
deficiency if neurologic?
B (1, 12) vit E
93
dopamine antagonists
antiemetic i.e. prochlorperazine have peripheral prokinetic effects --\> increase motility of the GI tract --\> increases rate of gastric emptying caution in patients w parkinsons!
94
soluble fiber
undigested until it reaches the colon includes pectins, guar gum used to thicken diarrhea
95
96
anticholinergics
systemic antidiarrheals increase intestinal muscle tone and peristalsis lots of side effects
97
prostiglandins
increased mucus and bicarb secretion increase mucosal blood flow
98
riboflavin
B6
99
manometry
primary tool to measure esophageal peristalsis record intraluminal pressure!
100
biphasic of h pylori
101
cyclin D1
HP can affect host cell genes in cell cycle •Diagram shows effect of helicobac on cyclinD1 expression oThis is one target gene shown as an ex but there are many others * When helicobac sees cells, it binds to cell, launch CagA appartatus, injects CagA, gets phosphorylated and interacts with MAP kinases (e.g. ERK1/2, p38, JNK) * MAPK phosphorylate transcription factors that work upstream of important genes like cyclin D1 that affect cell cycle progression This is another example of how HP is talking to human cells
102
chromium deficiency
glucose intoleance (high blood sugar) peripheral neuropathy
103
anticholinergics
antiemetic esp for vestibular and gi disorders
104
post absorptive phase of digestion
processing within enterocyte transport into blood stream and lymphatics
105
conditions of maldigestion
impaired nutrient hydrolysis lactose intolerance pancreatc insufficiency small bowel bacteria over growth bile acid deficiency
106
insoluble fiber
passes through intestine mostly unchanged includes lignin, cellulose used to treat mild constipation
107
extrinsic LES
diaphragmatic crural fibers anchored by phrenoesophageal ligament So, remember the LES is sort of a complex apparatus It’s made up of intrinsic components, so we have the smooth muscle layers of the lower esophagus coming down so that’s the longitudinal and circular muscle layers. And then there’s also an extrinsic component which is primarily made up of diaphragm so when there is no hernia or no sort of anatomical defect, this diaphragm contributes to the tone of the LES.
108
if beefy red tongue?
any of the Bs! 2, 3, 12 folate, protein, iron
109
B vitamin deficiency clinical signs
cheilosis (swollen lips), angular stomatitis (scaly only around nose) seborrheic dematitis anemia
110
gluten
storage protein in wheat, rye, barley rich in prolamine and glutamine which leads to incomplete digestion by intestinal enzymes long peptide results which passes through the epithelial barrier and triggers an immune reaction in genetically susceptible individuals
111
symptoms of diabetic gastroparesis
early satiety bloating nausea and vomiting occasional bezoar development (accumulated indigestable material)
112
Linzess
actiaves guanylate cyclase c receptor on lumenealsurface of intestinal epithelal cells - opens CFTR and Cl secretion happens
113
IBS-D
IBS with diarrhea
114
excitatory innervation in esophagus
more proximal
115
h pylori and ghrelin
more ghrelin without h pylori
116
copper deficiency
impaired bone density microcytic anemia
117
small intestinal bacterial overgrowth (SIBO)
excess build up of bacteria in upper small bowel bacteria deconjugates bile acids and leads to impaired fat processing and absorption
118
red flags for NOT IBS
weight loss nocturnal fam history of colon cancer blood mixed w stool recent abx
119
lactase deficiency
inadequate levels of lactase in BB lactase levels are highest after birth and decline after weaking without lactase, lactose is not broken down into glucose and galactose undigested lactose pulls water into lumen (osmotic) this lead to rapid transit into the colon - bacteria ferment lactose and generate gas primary = congenital , asians, africans, mediterranian secondary - infectious enteritis, celiac, ibd
120
gastroparesis cause
30% = long standing diabetes 30% idiopathic (post viral?) collagen vasc disease amyloidosis
121
harris benedict equation
energy requirements
122
functional esophageal disorders
heartburn chest pain dysphagia globus
123
hiatal hernia
GERD associated ## Footnote So you have the esophagus smooth muscle coming down here. This would be the intrinsic LES (black arrow) with longitudinal and circular muscle layers. But now it’s been displaced from the diaphragm. Since normally the diaphragm adds to its pressure, that makes it inherently low pressure here (at the LES). Not only that, you have acid production happening right here directly (lavender arrow) and you can see that that might make it a little more easy to have acid coming up A hiatal hernia (this is not a great picture of that), but it’s essentially when part of the stomach pushes up through the diaphragm and displaces the LES smooth muscle portion from the esophagus, from the diaphragm and sort of causes the whole apparatus to be a little bit separate and now you have acid production coming right here above the diaphragm and it can more easily come up.
124
NSAID ion trapping
wak acids! once ionized, NSAIDs remain water soluble and "trapped" inside cell
125
factors in early life that can contribute to IBS
abuse maternal deprivation GI infections abx microbiome early: diff factors cause development of abnormalities in ENS, visceral sensation, brain gut interactions, mental health later: common environmental triggers like food and stress
126
tissue injury in celiac
increased intraepithelial lymphocytes crypt hyperplasia villous blunting
127
thiamin
B1
128
functional gastrointestinal disorders
multidetermined disorders composite factors effect everything gut mucosa, microflora, ENS, extrinsic neural connections, signalling brain and sc
129
treatment of achalasia
\*decrease P in LES (gravity promotes emptying) 1. pharma (botox) 2. dilation of LES/surgical myotomy (cut through muscle) 3. POEM - balloon tipped catheter
130
131
vitamin A
retinol vision, immune function
132
osmotic laxatives
i.e. golytely (colo prep) hypertonic agents draw fluid into lumen by osmosis and cause diarrhea may cause electrolyte defects effect in 3 hrs
133
laxatives
production of a soft formed stool over a period of 1 day or more propmt fluid evacuation of the bowel - more intense for constimation (pain, decreaseamt of strai, pre-exams)
134
retching
labored rhythmic respiratory activity and abdominal contractions that usually precede vomiting builds up P gradient for vomiting
135
treatment of vomiting
treat complications (replace Na, water, K) identify and treat underlying cause if possible symptomatic relief preventative measures (cancer therapy)
136
antihistimines
i.e. meclizine esp for vestibular disorders antiemetic
137
CCK
triggered by dietary fat in duodenum 1. chyme entering duodenum causes enteroendocrine cells of the duodenal wall to release secretin but FATTY PROTEIN induces cck 2. cck and secretin enter blood stream 3. upon reaching pancreas, cck induces secretion of pancreatic juice (enzyme rich) - secretin causes more HCO3
138
GERD triggers
large meals fatty spicy acid foods bending, stooping, lying down frequency of reflux related symptoms varies widely lifting, staining, strenuous activities
139
adsorbants
pepto! anti-dairrheal coat the gut wall bnd to causative bugs or toxins and permit elimination
140
treatment of compilcated diverticulitis
abscess need to be drained and resect
141
selective serotinin RAs
esp to prevent chemo-induced nausea and vomiting
142
iron deficiency
facilitates oxygen delivery to tissue deficiency - microcytic anemia
143
zinc deficiency risk and symptoms
at risk if chronic diarrhea symp: scaly red rash around nose, mouth, eyes, groin diarrhea (viscous cycle) poor wound healing impaired immune decreased night vision altered taste
144
treatment for short bowel syndrome
antidiarrheal medications nutritional support - dietary interventions complicated cases could require intestinal transplant
145
causes of SIBO
stasis! from impaired motility or structural factors Stasis – slow motility (structural, things not moving) – post surgery, connection sit that’s a pocket
146
scintigraphy
gastric emptying - gold standard for gastroparesis solid/liquid emptying by radioloabeled meal measure every 15 min for 4 hours retention of \>10% of solids at 4 hours = diagnosis
147
conditions of malabsorption
\*\*impaired mucosal absorption of nutrients loss of SA (celiac, small bowel syndrome, radiation), impaired lymph transport
148
PUFA
omega 6 and omega 3 lineoleic and lineolenic essential FA can't be made
149
treatment of gastroparesis
correct nutritional issues/electrolte problems glucose control (if diabetic) consider meds
150
gastroparesis in diabetcs
commonly have aberrant fundic accomodation associated w dyspepsia and bloating
151
regurgitation
effortless movemeent of gastric contents toward the mouth without characteristic motor and autonomic changes seen w vomiting
152
types of glands in fundus
parietal chief endocrine mucus
153
vitamin c
collagen synthesis, wound healing
154
riboflavin
B2
155
diverticulosis epidemiology
age related! almost all in older people left sided in western right sided in asia and africa
156
short bowel with long ileal resection
bile acids are so poorly absorbed htat the liver can't synthesize enough to keep levels adequate leads to fat maldigestion and malabsorption restrict fat intake in diet supplement with MCT oil
157
lubricant laxative
i.e. stool softener (colace), mineral oil lubricates and softens stool retards water reabsorption works in 6-8 hrs little laxative effect lowers surface tension of stool allowing water to enter and softening!
158
antispasmodics
anticholinergics given based on the presuption that pain is due to intestinal spasm 0 minimally effective Bentyl, LEvsin
159
pellagra
B3 deficiency - dermatitis, diarrhea, dementia hyperpigmentation without uv exposure
160
GERD progression
normal inflammed baretts dysplasia adenocarcinoma So this slide I’ll get back into a little bit later, just to give an overview of what reflux disease can progress into. So, when you have a normal esophagus like in the video it should be looking sort of whitish, we say pearly white, the epithelium should be stratified squamous, and then, as acid starts to comes up into the esophagus over time, you can get the development of what’s called esophagitis. I’ll have another little video later, looking at that. And that’s really when your defense against acid in the esophagus is overwhelmed by the amount of reflux of acid up from the stomach and you can get esophagitis. On endoscopy it will look like this with sort of erosions and redness (erythema) coming out (pointing to second picture from left) And microscopically, there’s just a little more acid going through the layers. Over time that acid reflux esophagitis we think is really the next step into going into Barrett’s esophagus. Now what is Barrett’s esophagus, Barrett’s is when the actual squamous mucosa starts changing, it’s called metaplasia and we’ll get into that in detail a little bit later. But the mucosa essentially becomes specialized into intestinal metaplasia. So, it becomes columnar and starts looking almost like the small intestine After awhile, with prolonged acid in the esophagus with Barrett’s, the cells can become dysplastic which really is the next step into cancer. So classically, you know, what we think is with acid reflux over time there’s a chance the patients can go from normal to esophagitis, to Barrett’s to dysplasia and then finally adenocarcinoma.
161
quantitative fecal fat test
for fat malabsorbtion start 100g fat diet 2-3 days before study and continue through study collect stool over 72 hours if \>7 g of fat in stool per day
162
5-HT Agonists
Tegoserod accelerates gastric emptying and small bowel transit for constipation dominant IBS - side effect is mild diarrhea only if no response to fiber or laxatives
163
abdominal pain in IBS
visceral nerves affected pain is diffuse and poorly localized
164
acid pocket
reservoir from which reflux originates after a meal lag phase - food sits in fundus - why some more prone to GERD increase reflux if closer to esophagus can differ in patietns
165
treatment of uncomplicated diverticulitis
clear liquid diet antibiotics
166
antiemetics
anti-vomiting dopamine antagonists serotinin antagonists tricyclic antidepressants
167
Schilling test
assess cause of B12 deficiency 1. oral B12 and intramuscular B12 - asses absorption by measuring urinary excretion over 24 hours - if low proceed to part 2 to see if it's due to lack of IF 2. labeled B12 is given with IF - if urinary excretion is normal - the patient has perniscous anemia (IF deficiency) 3. give vit b12 and antibiotics - if normalizes, bacterial overgrowth is cause 4. give B12 and panc enzymes - if normalizes pancreatic insufficiency is the cause
168
celiac disease
autoimmune where gluten triggers an immune raeaction that damages the small intestinal lining
169
functional gastroduodenal disorders
dyspepsia nausea vomiting
170
functional anorectal disorders
defectation disorders fecal incontenance anorectal pain
171
most common causes of peptic ulcer disase
h pylori NSAIDs
172
GERD alarm symptoms
dysphagia bleeding weight loss chest pain
173
gastric slow waves
always present, regular electrical pattern (produced by ICC!) propigate circumerentially and migrate toward pylorus do not lead to contractions by themselves! contractions occur on crests of slow waves max contractions is directly related to slow wave frequency
174
deficiency if joint pain/weakness?
vit c
175
complication of achalasia
aspiration pneumonia esophageal cancer risk (squamous - stasis esophagitis, adeno - GERD after LES disruption)
176
CagA
h pylori ## Footnote HP produces protein called CagA and has type 4 secretion system used to export CagA and other materials from HP and directly inject into epithelial cells * CagA has tyrosine phosphorylation domains that are recognized by host cell kinases like Sarc and Abl * Phosphorylated protein [blue blob labeled Y-P] has many different activities within epithelial cells * HP has whole repertoire of CagA or no CagA that signal the host in different ways
177
gastric lag phase
most solids stay in proximal stomach for 30-60 min contractions then get food toward antrum
178
features of achalasia
incomplete relaxation of LES causes functional obstruction of esophagus until hydrostatic P \> LES P dysphagia liquids/solids difficulty belching weightloss, CP, heart burn
179
5-HT antagonists
\*\*diarrhea predominant IBS! receptors on ENS sensory neurons slow colonic transit and increase colonic compliance reduce intestinal sensitivity to distention
180
types of unsaturated fats
MUFA - omega 9 PUFA - omega 6 and omega 3 (lineoleic and lineoenic) - essecntal FA and can't be made
181
octreotide (sandostatin)
mimis somatostatin inhibits secretion of gastrin, cck, glucagon, gh, insulin, secretin reduces secretion offluids and motility
182
luminal phase of digestion
intraluminal substrate hydrolysis by various enzymes maldigestion when abberant!
183
Nucleus tractus solitarius
may serve as central pattern generator for vomiting and taking in input via area postrema then project to various motor nuclei in the vomiting reflex