Unit 1- GI Flashcards
Histo info
digest things “outside” of body/cells then absorb
Histo GI layers
mucosa (incl epithelium, lamina propria, then muscularis mucosa)
submucosa
muscularis propria
adventitia
mucosa layer mucins glands lamina propria muscularis mucosa
wavy epithelial surface on top of basal lamina
-barrier is selective for certain molecs
surface: mucins
heavily glycosylated (Ser; Thr) w/ sugars and -OH groups (hydrated) and disulfide bonds
-highly resistant to digestion
glands: mucosal glands (and submucosal glands) accessory glands (ex pancreas) completely outside of mucosa/submucosa
Loose CT- lamina propria
- lots of capillaries
- lots of lymphocytes around the capillaries (even more toward colon)- mostly producing IgA
smooth muscle layer- muscularis mucosa
thickness depends on where you are in GI
demarcates mucosa and submucosa
submucosa
muscle layers
serosa
nerve plexi
more dense CT
can have glands
outside: most of the GI has smooth muscle layers- “inner circular” and “outer longitudinal” layers
- stomach has additional oblique muscular layer
very outside: serosa: adventitia w/ large blood vessels and large nerves; has mesothelial layer around it; (all places except esophagus have serosa)
Meissner’s plexus: nerve plexus running in here to stimulate the muscularis mucosa and glandular secretions
Auerbach’s plexus: runs between inner circular and outer longitudinal layers
M cells
enteroendocrine cells
M cells:
survey things in gut- lots of sampling components (antigens, nl flora)
-fast response w/ macrophages and local immune responses if epi layer or integument is compromised
Enteroendocrine cells:
secrete into the local blood supply
-secrete Gastrin, Polycystikinan, and Secretin
stomach mucosa histo
gastric gland cells
thick mucosa that has GLANDS that come in and branch deep into mucosa
ascinar cells at the end of the branches
glandular
gastric gland-
3 main types of cells here
runs all the way down to the muscularis mucosa
1 cell in neck at top: goblet (mucus secreting cell)
another cell- parietal cell (fried egg; prod HCl)
- large canaliculi
- proton pump to acidify stomach
- large SA; lots of mito
chief cells- at bottom; prod pepsinogen (zymogen); activated in low pH
enteroendocrine cell- not much contact w/ luminal surface; secretes into blood via basolateral side (prod gastrin)
this is all within the lamina propria
muscularis mucosa squeezes to help glands move things out as it contracts
intestine histo
SI vilar surface lined by epithelium large SA for abs at the ends we have small microvillar surface called enterocytes- large SA for Na/K ATPase to take up molecs
Crypts:
Crypts of Lieberkuhn (esp defined in SI)
-special Paneth cells (granular); prod Defensins- antibacterial and lysozyme; primarily involved in preventing bac growth if it makes it alive to duodenum
extend into submucosa via Brunner’s glands- primarily prod NaHCO3- only found in duodenum
intestinal ridges: plicae circularis (inc SA by 2-3 fold)
Jejunum has plicae circularis and crypts of Lieberkuhn
Ileum has peyer’s patches (lymphoid aggregates)
Colon:
thick mucosa
number of linear, highly regular crypts filled w/ mucus secreting cells (test tube rack)
goblet cells for lube
absorb water and salts
conc fecal matter
still have muscularis mucosa, and lamina propria and lymphocytes
-layer underneath: adipose cells mixed/ w/ some muscle strands
serous demilune- help flush water material into duct
can have myoepithelial cells arranged in web around individual acinar cells- contract to help force components out of individual acinar cells
esophagus histo
transition to stomach
has mucosal layer- mainly protective (not digestion)
inner circular and outer longitudinal muscle layers
skeletal muscle at top 1/3 and smooth muscle at bottom 1/3; mix in between
transition to stomach:
contraction of diaphragm mainly keeps the separation largely constricts; not really a sphincter there
stomach regions sphincters reservoir and pump funcs nl HCl acid secretion protection injury
cardia, corpus, pylorus
true sphincter- pyloric sphincter (to duodenum)
allows stomach to have low pH to denature proteins and prevent unwanted flow to duodenum
Reservoir and pump function o receptive relaxation ♣ fundus o solid emptying ♣ vagally-mediated contractions o residual solids emptied ♣ During non-fed state by MMC every 90-120 min
nl HCl acid secretion o Acid secretion: ♣ Denature proteins ♣ Protect from infection ♣ Aids in abs of iron and vit B12 o Mediated by ♣ Neural, hormonal, and paracrine pathways
protection
surface mucus secretion, bicarbonate secretion into mucus; mucosal blood flow; epithelail barrier func; epi regenerative capacity; elaboration of prostaglandins
Injury, ischemia, shock, NSAIDs can alter the protective mech’s of the stomach
lymphatic channel
in the center of lamina propria and going into submucosa- lymphatic channel called lacteal
all throughout villus and mucosa
-lots of capillaries for large blood flow
water goes into lacteal
any fats we take up to into lacteal as chylomicrons
enterocytes are involved in syn as those triglycerides as the monoglyceride fats come across the cell
-have to digest then rebuild triglycerides to not clog things up
enzyme proteins at surface
enterokinase- proteolytic enzyme (not a phosphorylizer as the name implies) acts on trypsinogen from the pancreas converted to trypsin and activates the other zymogens that are also coming from pancreas
pancreas enzymes0 usually optimal at pH 7
lactase:
converts lactose to glucose and galactose
maltase-
breakdown of maltose into glucose
sucrose-
breaks down sucrose into fructose and glucose
these are cell surface proteins because don’t want to lose sugar proteins to bac
transport sugars, AAs, and other things to lacteals
bile salts from gallbladder/liver
important for emulsifying fats
wedge-shaped
polar ends, fit into lipid regions
lipases can degrade the lipases
what causes GI motility disorders
4 things
ENS-
missing, immature, damaged by infection, influenced by chem sub’s (inside and outside) = neuropathic
neurons
Diseased GI muscles
genetic defect (muscular dystrophy) or acquired (progressive systemic sclerosis) = myopathic
muscles
Abnormalities of intestinal cells of Cajal
pacemaker (Stims baseline contraction)
CNS disorders
-signals from CNS are impaired
esophageal manometry
used to dx esophageal disease
-visually highlight disorders
-esophageal pressure waves during swallowing- measure func
-swallow repetitively to measure P transmitted throughout;
looking at contraction/relaxation of UES and LES
esophagus-
dysphagia and heartburn
achalasia
no LES relaxation
absence of peristalsis
achalasia- hallmark of esophageal motility disorder (get dysphasia)
esophagus-
scleroderma/progressive systemic sclerosis PSS
multi sys disorder:
- obliterative small vessel vasculitis
- CT proliferation w/ fibrosis of multiple organs
GI manifestations 80-90%
-principal path’s are SM atrophy and gut wall fibrosis (predominately myopathic process)
characteristic “weakness of esophageal muscle disorder”
esophageal manifestations:
SM atrophy- weak peristalsis - dysphagia
SM atrophy- weak LES- GERD
unrepentant GERD- esophagitis - stricture
see nl high pressure in UE (striated, not smooth muscle); then absence of peristalsis and weak LES
esophagus- spastic disorders
uncertain etiology;
peristalsis preserved
symptoms usually chest pain and dysphagia
pathophys related to overactivity of excitatory nerves (an impairment of inhib innervations or overactivity of SM response)
gradient of excitatory/cholinergic and inhib/noncholinergic nerves in SM portion of esophagus
-greater conc of inhib nerves distally; overtime of activity or absence of inhibition
jackhammer esophagus on imaging
stomach- gastric motility
gastric pacemaker
interstitial cells of Cajal
proximal body along greater curvature
funds and proximal body
storage
low P to receive food- relaxation
distal body and antrum
-processing/grinding
emptying
stomach- emptying and reservoir func
emptying: receptive relaxation (vagally mediated inhib of body tone)
liquid emptying by tonic P gradient
solid emptying by vagally-mediated contractions
residual solids emptied during non-fed state by MMC every 90-120 min
reservoir:
receptive relaxation
-swallowing-induced vagal response
accommodation
-SM relaxation elicited by mechanical distention of stomach (gastric mechanoreceptors)
vasovagal response
gastroparesis
clinical manifestations
major causes
Dx
management
stomach paralysis
impaired transit of food from stomach to duodenum
(mechanical obstruction of gastric outlet excluded)
clinical manifestations: N/V early satiety postprandial abdominal distention postprandial abdominal pain
major causes
idiopathic (post infectious?)
post surgical (vagal nerve injury)- gastric, esophageal, thoracic surgeries: lung tx
diabetic
med-related (opiates)
others (rheum, paraneoplastic, neuro, myopathic- scleroderma!)
dx
gastric emptying study
Gastric scintigraphy: low fat EggBeaters radio labeled w/ Technetium 99
abnl: retention >60% at 2 hr or >10% at 4 hrs
management lifestyle/dietary (small and freq meals; low fat and low-residue diet; glucose control in diabetes) meds (pro kinetics; antiemetics) gastric electric stim surgery (2%)
SI nl
fed state
fasted state
~21 ft long; ~1 in diameter
fed state: primary motility is segmentation
9-12 contractions/min (pacemaker cells)
total transit time 3-5 hrs
fasted state: migrating motor complex sequential orderly short peristaltic waves stomach--> caudally sweep gut between meals
small bowel motility disorders
neuropathic
myopathic
CIPO
neuropathic:
nl amplitude of contractions but sustained bursts of uncoord phasic contractions
early return of MMC (migrating motor complex)
inc freq of MMC
myopathic
dec amplitude of contractions or complete lack of any motor activity
some diseases have feature of both
chronic intestinal pseudo-obstruction- CIPO
signs/symptoms of mechanical obstruction of SI without a lesion obstructing flow of contents
characterized by presence of dilation of bowl on imaging
major manifestation of SI dysmotility
SI bac overgrowth is a complication of CIPO: stasis –> bac overgrowth–> fermentation and malabs
symptoms:
N/V 83%
abd bain 74
distention 57
constipation 36
diarrhea 29
urinary Sx 17
etiologies of small bowel motility disorders and CIPO
neuropathic
mixed myopathic and neuropathic
CIPO (child vs adult)
neuropathic: degenerative neuropathies (Parkinson) paraneoplastic autoimmune (anti-Hu Ab) Chagas disease: parasite Trypanosome Cruzi Diabetes assoc (neuropathy)
Mixed myopathic and neuropathic
- infiltrative conditions (Scleroderma*, amyloidosis, eosinophilic gastroenteritis)
- idiopathic
CIPO- diff for children/adults
child:
mostly congenital
mostly primary condition (visceral neuroapthy/myopathy)
absent MMC predicts need for IV nutrition
-1/3 infants die w/in 1st yr of life
colon func
transport, store, and expel stool after absorbing majority of luminal fluid
2 types of motor activity
low amplitude tonic and phasic contractions for mixing luminal contents (Haustra)
high amplitude propagated contractions (HAPCs) for propelling
colonic motility inc after meal (gastrocolonic response) and on awakening