Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI 1 > GI Pathophysio > Flashcards

GI Pathophysio Flashcards

1
Q

vitamin a deficiency

A

night blindness

bitot spos (squamous cell prolif)

corneal perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How to diagnose diverticulitis

A

clinical if mild

CT scan or ultrasound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

epithelium of the stomach

A

simple layer of columnar epithelial cells

secrete mucus and bicarb

pits provide glands access to the lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

symptoms of pancreatic exocrine insufficeincy

A

bulky foul smelling stool

oily residue in toilet water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

NSAIDs and ulcer formation

A

decrease mucin and HCO3 so HCl can touch the cell

injury to cell - HCl can get closer!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

IBS-C

A

IBS with constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

consequences of bacterial overgrowth

A

unconjugate bile acids

use vit b12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

treatment of pancreatic exocrine insufficiency

A

pancreatic enzyme supplements wiht food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

viberzi

A

binds to opioid receptors in GI tract controling motility and hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

types of glands in the cardia

A

branched and tortuous

mucus

endocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

esohageal peristalisis in smooth muscle

A

inhibition followed by excitation

gradient of increasing inhibition (latency gradient)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

beri beri

A

B1 deficiency

dry - peripheral neruopathy

wet - CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

vitamin d deficiency

A

bone demineralization

hypocalcemia, hypophosphatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

uncomplicated diverticulosis

A

asymptomatic - incidental, increase fiber

symptomatic - bloating, constipation, passage of mucus, like IBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

bethanechol

A

prokinetic

muscarinic receptor agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Cholestyeramine (questran)

A

bile acid sequentrant, prevent reabsorption

bile acids, once complexed, are secreted in feces

lower plasma cholesteral

used to prevent diarrhea pst ileal resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

d-xylose test

A

for carb malabsorption

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

sibship size and gastric cancer risk

A

higher risk of cancer in later bown

higher risk with brothers and sisters

early years of life affect health decades later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

gastric motility of liquids

A

rapidly disperse through stomach and empty without delay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

prokinetics

A

Prokinetics help strengthen the lower esophageal sphincter (LES) and cause the contents of the stomach to empty faster.

more gerd?

combined prokinetic/amtoe,etoc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

mixed micelles

A

transport lipolytic products (mostly fA and MG)

hydrophilic part on outside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

vitamin K

A

dietary from plants, synthesize by gut bacteria

essential to function of blood clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

bulk laxatives

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

stimulant laxatives

A

derivatives of phenolphtalein

induce high amplitude propagated colonic contracts

appear to be safe!

rescue agents when no BM for several days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

opiates

A

systemic antidiarrheals

slow peristalsis - allow increased water reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

gastric motility of solids

A

lag phase then trituration

rate depends on nutrient content too (fat is slowest)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

fundoplication

A

surgical repair for hiatal hernia

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how to diagnose gastroparesis

A

EGD to r/o obstruction

scintigraphy = gold standard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

IBS pathophysiology

A

genetic/social factors + food and stress lead to symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

pseudoachalasia

A

malignancy (gastric)

paraneoplastic

chagas

eosinophilic gastroenteritis

infiltrative process at LES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

tissue transglutaminase

A

deamidates or crosslinks gliadin - increasing its affinity for receptors on WBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

folate

A

DNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

pathogenesis of diabetic gastroparesis

A

chronic hyperglycemia –> neuropathic changes and dysfunctional innervation through the vagus –> delayed gastric emptying due to autonomic neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Transient lower esophageal sphincter relaxations (TLESR)

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Barrett’s Esophagus

A

in response to acid reflux normal squamous epithelium may be replaced by columnar epithelium of the specialized intestine type

1% chance of adenocarcinoma (increasing!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

serotonin

A

imp NT and gut signaling molecule

major modulator brain-gut communication

activates enteric neurotransmission to initiate peristalsis and secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

selenium deficiency

A

cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

vitamin E

A

anti-oxidant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

short bowel with SHORT ileal resection

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

percent weight loss

A

(UBW - Actual BW)/UBW x 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

3 hypotheses of diverticuli

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

hydrogen breath test

A

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 –

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

short bowel syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

niacin

A

B3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

fundic accomodation

A

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

h pylori and esophageal disease

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

vitamin e deficiency

A

hemolytic anemia

neuro (ataxia, peripheral neuropathy, myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

if eye or vision problems?

A

vit A

zinc 9f night blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Treatment for SIBO

A

antibiotics

correct underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

mucosal phase of digestion

A

brush border hydrolysis

transport into epithelial cells (enterocytes)

when abberent - malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

reciporcal relationship between adenocarcinomas of stomach and esophagus

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

if oily scaling around nares?

A

riboflavin or zinc deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

treatment of IBS

A

mutlidiscplinary

education and reassurance

dietary (avoid exacerbations w lactose, low FODMAP diet)

stress management

meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

how to diagnose achalasia?

A

endoscopy (not swallowing)

barium swallow

manometry** gold standard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

gliadin

A

one of two types of protein that are components of gluten in wheat

contains the toxic AA sequences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

secretagoges

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

pantothenic acid

A

B5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

HLA DQ2 and HLA DQ8

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

adherence pedistal

A

h pylori forms with epithelial cell to insert proteins

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

colonic diverticulosis

A

sac like protrusion of the colonic wall

mucosa and submucosa herniate through the muscularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

intrinsic LES

A

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
Q

symptoms of SIBO

A

gas/bloat

diarrhea

maybe B12 deficiency? Bacteria uses B12

76
Q

treatment for lactase deficiency

A

limit lactose containing foods

use lactase supplements

77
Q

esophageal cancer and cancer

A

adenocarcinoma!

78
Q

vitamin c deficiency - clinical manifestations

A

swollen bleeding gums

loose teeth

petechiae

periungal hemorrhage

impaired wound healing

arthalgias, joint effusions

corkscrew hair

anemia

79
Q

cause of achalasia

A

uncertain

autoimmune?

altered inhibitory innervation of smooth muscle

loss of peristalsis

failure of les relaxation

80
Q

tricyclic antidepressents

A

IBS

inhibitory effect on gut - alleviate symptoms at a very low dose

*amitripyline - take at sub depression levels

81
Q

IBS-M

A

constipation and diarrhea

82
Q

the bowel disorders

A

IBS

functional diarrhea

functional constipation

83
Q

inhibitory innervation in the esophagus

A

more distal

84
Q

how do you diagnose pancreatic exocrine insufficiency?

A

fecal elastase level -

Stool test – elastase – if enough pancreatic enzymes are in bowel and going into stool

Stool test to measure amt in the stool

85
Q
A
86
Q

types of glands in antrum

A

endocrine

mucus

g cells (gastrin)

87
Q

impedence-pH monitoring

A

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
Q

area postrema

A

has chemoreceptor trigger zone (CTZ) sensitive to many stimuli

89
Q

diverticulitis

A

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
Q

cobalamin

A

B12

91
Q

h pylori induces what kind of cancer?

A

adenocarcinoma

92
Q

deficiency if neurologic?

A

B (1, 12)

vit E

93
Q

dopamine antagonists

A

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
Q

soluble fiber

A

undigested until it reaches the colon

includes pectins, guar gum

used to thicken diarrhea

95
Q
A
96
Q

anticholinergics

A

systemic antidiarrheals

increase intestinal muscle tone and peristalsis

lots of side effects

97
Q

prostiglandins

A

increased mucus and bicarb secretion

increase mucosal blood flow

98
Q

riboflavin

A

B6

99
Q

manometry

A

primary tool to measure esophageal peristalsis

record intraluminal pressure!

100
Q

biphasic of h pylori

A
101
Q

cyclin D1

A

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
Q

chromium deficiency

A

glucose intoleance (high blood sugar)

peripheral neuropathy

103
Q

anticholinergics

A

antiemetic

esp for vestibular and gi disorders

104
Q

post absorptive phase of digestion

A

processing within enterocyte

transport into blood stream and lymphatics

105
Q

conditions of maldigestion

A

impaired nutrient hydrolysis

lactose intolerance

pancreatc insufficiency

small bowel bacteria over growth

bile acid deficiency

106
Q

insoluble fiber

A

passes through intestine mostly unchanged

includes lignin, cellulose

used to treat mild constipation

107
Q

extrinsic LES

A

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
Q

if beefy red tongue?

A

any of the Bs! 2, 3, 12

folate, protein, iron

109
Q

B vitamin deficiency clinical signs

A

cheilosis (swollen lips), angular stomatitis (scaly only around nose)

seborrheic dematitis

anemia

110
Q

gluten

A

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
Q

symptoms of diabetic gastroparesis

A

early satiety

bloating

nausea and vomiting

occasional bezoar development (accumulated indigestable material)

112
Q

Linzess

A

actiaves guanylate cyclase c receptor on lumenealsurface of intestinal epithelal cells - opens CFTR and Cl secretion happens

113
Q

IBS-D

A

IBS with diarrhea

114
Q

excitatory innervation in esophagus

A

more proximal

115
Q

h pylori and ghrelin

A

more ghrelin without h pylori

116
Q

copper deficiency

A

impaired bone density

microcytic anemia

117
Q

small intestinal bacterial overgrowth (SIBO)

A

excess build up of bacteria in upper small bowel

bacteria deconjugates bile acids and leads to impaired fat processing and absorption

118
Q

red flags for NOT IBS

A

weight loss

nocturnal

fam history of colon cancer

blood mixed w stool

recent abx

119
Q

lactase deficiency

A

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
Q

gastroparesis cause

A

30% = long standing diabetes

30% idiopathic (post viral?)

collagen vasc disease

amyloidosis

121
Q

harris benedict equation

A

energy requirements

122
Q

functional esophageal disorders

A

heartburn

chest pain

dysphagia

globus

123
Q

hiatal hernia

A

GERD associated

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
Q

NSAID ion trapping

A

wak acids!

once ionized, NSAIDs remain water soluble and “trapped” inside cell

125
Q

factors in early life that can contribute to IBS

A

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
Q

tissue injury in celiac

A

increased intraepithelial lymphocytes

crypt hyperplasia

villous blunting

127
Q

thiamin

A

B1

128
Q

functional gastrointestinal disorders

A

multidetermined disorders

composite factors effect everything

gut mucosa, microflora, ENS, extrinsic neural connections, signalling brain and sc

129
Q

treatment of achalasia

A

*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
Q
A
131
Q

vitamin A

A

retinol

vision, immune function

132
Q

osmotic laxatives

A

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
Q

laxatives

A

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
Q

retching

A

labored rhythmic respiratory activity and abdominal contractions that usually precede vomiting

builds up P gradient for vomiting

135
Q

treatment of vomiting

A

treat complications (replace Na, water, K)

identify and treat underlying cause if possible

symptomatic relief

preventative measures (cancer therapy)

136
Q

antihistimines

A

i.e. meclizine

esp for vestibular disorders

antiemetic

137
Q

CCK

A

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
Q

GERD triggers

A

large meals

fatty spicy acid foods

bending, stooping, lying down

frequency of reflux related symptoms varies widely

lifting, staining, strenuous activities

139
Q

adsorbants

A

pepto!

anti-dairrheal

coat the gut wall

bnd to causative bugs or toxins and permit elimination

140
Q

treatment of compilcated diverticulitis

A

abscess

need to be drained and resect

141
Q

selective serotinin RAs

A

esp to prevent chemo-induced nausea and vomiting

142
Q

iron deficiency

A

facilitates oxygen delivery to tissue

deficiency - microcytic anemia

143
Q

zinc deficiency risk and symptoms

A

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
Q

treatment for short bowel syndrome

A

antidiarrheal medications

nutritional support - dietary interventions

complicated cases could require intestinal transplant

145
Q

causes of SIBO

A

stasis!

from impaired motility or structural factors

Stasis – slow motility (structural, things not moving) – post surgery, connection sit that’s a pocket

146
Q

scintigraphy

A

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
Q

conditions of malabsorption

A

**impaired mucosal absorption of nutrients

loss of SA (celiac, small bowel syndrome, radiation), impaired lymph transport

148
Q

PUFA

A

omega 6 and omega 3

lineoleic and lineolenic

essential FA can’t be made

149
Q

treatment of gastroparesis

A

correct nutritional issues/electrolte problems

glucose control (if diabetic)

consider meds

150
Q

gastroparesis in diabetcs

A

commonly have aberrant fundic accomodation

associated w dyspepsia and bloating

151
Q

regurgitation

A

effortless movemeent of gastric contents toward the mouth without characteristic motor and autonomic changes seen w vomiting

152
Q

types of glands in fundus

A

parietal

chief

endocrine

mucus

153
Q

vitamin c

A

collagen synthesis, wound healing

154
Q

riboflavin

A

B2

155
Q

diverticulosis epidemiology

A

age related! almost all in older people

left sided in western

right sided in asia and africa

156
Q

short bowel with long ileal resection

A

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
Q

lubricant laxative

A

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
Q

antispasmodics

A

anticholinergics

given based on the presuption that pain is due to intestinal spasm 0 minimally effective

Bentyl, LEvsin

159
Q

pellagra

A

B3 deficiency - dermatitis, diarrhea, dementia

hyperpigmentation without uv exposure

160
Q

GERD progression

A

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
Q

quantitative fecal fat test

A

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
Q

5-HT Agonists

A

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
Q

abdominal pain in IBS

A

visceral nerves affected

pain is diffuse and poorly localized

164
Q

acid pocket

A

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
Q

treatment of uncomplicated diverticulitis

A

clear liquid diet

antibiotics

166
Q

antiemetics

A

anti-vomiting

dopamine antagonists

serotinin antagonists

tricyclic antidepressants

167
Q

Schilling test

A

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
Q

celiac disease

A

autoimmune where gluten triggers an immune raeaction that damages the small intestinal lining

169
Q

functional gastroduodenal disorders

A

dyspepsia

nausea

vomiting

170
Q

functional anorectal disorders

A

defectation disorders

fecal incontenance

anorectal pain

171
Q

most common causes of peptic ulcer disase

A

h pylori

NSAIDs

172
Q

GERD alarm symptoms

A

dysphagia

bleeding

weight loss

chest pain

173
Q

gastric slow waves

A

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
Q

deficiency if joint pain/weakness?

A

vit c

175
Q

complication of achalasia

A

aspiration pneumonia

esophageal cancer risk (squamous - stasis esophagitis, adeno - GERD after LES disruption)

176
Q

CagA

A

h pylori

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
Q

gastric lag phase

A

most solids stay in proximal stomach for 30-60 min

contractions then get food toward antrum

178
Q

features of achalasia

A

incomplete relaxation of LES causes functional obstruction of esophagus

until hydrostatic P > LES P

dysphagia liquids/solids

difficulty belching

weightloss, CP, heart burn

179
Q

5-HT antagonists

A

**diarrhea predominant IBS!

receptors on ENS sensory neurons

slow colonic transit and increase colonic compliance

reduce intestinal sensitivity to distention

180
Q

types of unsaturated fats

A

MUFA - omega 9

PUFA - omega 6 and omega 3 (lineoleic and lineoenic) - essecntal FA and can’t be made

181
Q

octreotide (sandostatin)

A

mimis somatostatin

inhibits secretion of gastrin, cck, glucagon, gh, insulin, secretin

reduces secretion offluids and motility

182
Q

luminal phase of digestion

A

intraluminal substrate hydrolysis by various enzymes

maldigestion when abberant!

183
Q

Nucleus tractus solitarius

A

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

GI 1 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions