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92 Cards in this Set

  • Front
  • Back

GI tract 4 layers

MUCOSA (lumen side)




SUBMUCOSA




MUSCULARIS EXTERNA




SEROSA or ADVENTITIA

Mucosa

3 layers




Epithelium


lamina propria (thin layer of CT)


muscularis mucosa (1-2 layers of SM)

2 layers of muscularis externa

inner: circular


outer: longitudinal

serosa vs adventitia for outside layer (dense CT)



serous membrane=visceral peritoneum




adventitia=retroperitoneal parts

UES



upper esophageal sphincter


skeletal muscle


involved in deglutition reflex (swallow)


contr'd by CN 9, 10, 12


normally closed, only relaxes (opens) for bolus




main fxn: prevent backflow of food from esoph to pharynx


involved in eructation (burping)

trigger peristalsis in esoph

bolus present--->stretch pharynx tactile receptors




from pharynx to esophagus: pharyngeal peristalsis


down esophagus: esophageal

LES

gastroesophageal sphincter


(lower esoph)


Smooth muscle


prevent reflux of gastric contents into esoph


normally, relaxes (opens) when bolus reaches gastroesoph jxn



two most common clinical problems with LES

Achalasia


GERD

Achalasia

failure to relax LES


cant open LES! (stays closed) food accum in esoph cant empty into stomach


common sx: regurgitation (into mouth)


dysphagia (trouble swallowing)


inflamm




confirm? x ray: esophagram


(pic with barium probed food so lit up all accumulated in bottom of esophagus, shows food stuck there not emptying)


dilated proximal esophagus and narrow tapering of distal esophagus=birds beak sign

GERD

Gastro-esoph reflux disease


occurs if LES is incompetent=stays open (wont close!)


acidic contents of stomach back into distal esoph---->esoph damage=barrets esoph




most common sx: heartburn,


substernal chest pain


(nausea, regurg, dysphag, etc.)




most common diagnostic: endoscopy: esophagoggastroduodenoscopy (EGD)







stomach

j shaped sack left upper quadrant


under diaphragm


HCl, chemical digestion begins in stomach.


bolus turn to chyme




internal surface lined with simple columnar epithelium with goblet cells


small invaginations of epithel into mucosa=gastric pits or foveolae




two borders of stomach (curvatures):


medial border=lesser curvature (lil concave side facing medially)


lateral border-greater curvature (convex side facing lat left side of abdominal cav)



when stomach is empty the mucosa of internal surface of stomach make

rugae: rough irregular longitudinal folds




rugae permit expansion of stomach as it fills

4 parts of stomach

cardia: part closest to esoph


(part right from when esophagus and LES meet beginning of stomach=cardia) lil beginning of stomach section



fundus: top of stomach closest to diaphragm


(that top bump)




body: biggest middle part




pylorus: last bottom part before connection to duodenum (further divided into antrum and canal)



pylorus

(after body of stomach is over the pylorus is last part of stomach before duodenum)


divided into


pyloric antrum, where stomach turns to the right like bottom part start curving medially (which is to the right cuz we are on the left)




pyloric canal, where stomach becomes narrower, end of stomach part right before duod




pyloric canal ends with pyloric sphincter aka gastroduodenal sphincter (separate stomach from duod)

parietal cells

of stomach


aka oxyntic cells


produce HCl


produce IF (essential for b12 absorpt)

cheif cells

of stomach


produce pepsinogen (zymogen converted to pepsin in presence of HCl)



Pepsin

breaks down peptide bonds in proteins

when stomach contents processed into chyme and pass thru pyloric sphincter into duodenum

brunners glands of duod secrete alkaline secretion to neutralize the chyme





pylorospasm

failure of pyloric sphinter to relax (cant open) (food cant pass from stomach to duod)




usually transient, imperfect neuromuscular regulation of pyloric sphincter




more common in kids than adults -->congenital pyloric stenosis

congenital pyloric stenosis

abnormal dvlpmnt of pyloric sphincter


permanent!


doesnt allow for passage of food at all


usual presentation: non bilious projectile vomiting w/in first week of life


requires surgical repair

gastritis

inflammation of stomach mucosa


two types of chronic gastritis: type a, type b




can lead to peptic ulcer

type a gastritis

autoimmune


inflammation of mucosa in fundus and body of stomach




autoimmune destruction of parietal cells producing hcl and if cause low stomach juice acidity (achlohydria which is hi stomach ph) and no IF leading to b12 avitaminosis which leads to pernicious anemia (macrocystic/megaloblastic anemia); giant rbc's




type a is autoimmune and anemia

type b gastritis

involves inflammation of mucosa in antrum and pylorus of stomach


caused by H pylori infection (surive in high acidity environment of stomach), destroy stomach mucosa




type b is bacterial

peptic ulcer

caused by chronic gastritis and loss of mucosa




big lesion of mucosa leaving underlying tissues to be digested by stomach acid and enzymes




sx: burning/gnawing epigastric pain, nausea, hematemesis (vomiting blood) and melena (blood in stool)




PUD include both gastric and duodenal ulcers




gastric ulcers vs duodenal ulcers

gastric PUD

Pain worse with meal = incr'd gastric acid


pyloric region most common region


ulcers can perforate the wall: erosion of gastric arteries


post. wall ulcers can erode pancreas




can cause hematemesis

duodenal PUD

4 times as many more ulecers here than in stomach. usually benign


Pain improves with meal =incr'd duodenal bicarbonate


ulcers can perforate wall: erosion of gastroduodenal artery with severe bleeding




can cause hematochezia

coming down descending aorta we get to celiac trunk

3 branches off celiac trunk


left gastric artery the split between the two other splits that will go up towards left top stomach (cardia)


splenic artery the big split going left behind stomach to spleen


hepatic artery the big split going to right (medially)

left gastric artery

runs thru lesser omentum and supplies cardia and lesser curvature of stomach


(so it comes off celiac trunk, goes up to left top of lesser curve and runs along side cardia and then lesser curvature)




it anastomoses on the right after it curves with the right gastric artery

right gastric artery

a branch off the common hepatic artery


comes up off hepatic and goes down to lesser curvature to connect with left gastric along the curve

left gastro omental (gastro-epiploic) artery

terminal branch of the splenic artery that supplies the greater curvature of stomach


(so it came off splenic which was running behind stomach all the way to lateral left side, it goes down along greater curv)


it runs thru greater omentum

right gastroomental artery

terminal branch of hepatic artery that will anastomose with left gastro omental art on greater curvature


(it went from common hepatic art to gastroduod art then its the right gastro-omental)

common hepatic artery

Big branch off celiac trunk that goes right



It's branches:


the two proximal branches (proximal to celiac trunk-est)


right gastric artery (going to lesser curv)


gastroduodenal artery that turns into or branches into right gastro-omental artery (going to greater curv)



then distal further from celiac trunk we have branches off hepatic artery-


cystic artery,


left and right hepatic arteries

off the gastroduodenal artery

right gastro-omental (same as gastroepiploic)


superior pancreaticoduodenal

mesentery

double layer of visceral peritoneum holding organ to dorsal wall




root of mesentary from left side of L2 to sacroiliac joint




mesentary that holds large instestine= mesocolon


transverse mesocolon splits the abdominal cavity into supracolic compartment (liver, stomach, spleen) and infracolic (intestines)



omentum

double layer of visceral peritoneum connecting organ to organ




"policeman of the abdomen" cuz it can fill voids if something removed/ in the wrong place




it's the vascularized fat flap covering intestines first seen on opening abdomen




lesser omentum: draping from liver to stomach (so from under liver to lesser curvature of stomach connect)




greater omentum: from stomach greater curvature side (underside) and over the segment of colon in upper abdomen

duodenum

first part of small intestine, c shaped part


retroperitoneal




contains brunner glands: produce mucus rich alkaline secretion that contains bicarbonate and neutralizes acid coming from stomach




consists of 4 parts


superior


descending (where bile enters via sphincter of oddi)


horizontal


ascending




the last 3 parts (everything except superior) have no mesentary and are immobile




end of duodenum is a sharp bend known as duodenojejenal flexure

jejenum

thicker and more vascular and redder than duod or ileum


mostly lies in umbilical region


has highest activity of brush border enzymes


responsible for absorption


surface increased by presence of many vili and plicae circularis (aka intestinal valves), permanent large, tall closely spaced circular folds running around lumen of jejenum and ileum




the jej compared to il:


less complex arterial arcades


longer vasa recta


more plicae circularis, thicker, more highly folded


no fat in mesentery







ileum



il compared to jej:


longer/more arterial arcades


shorter vasa recta


less plicae circularis, thinner less folded


fat is present in mesentery




short fat il kids go to the arcade




ileum is last and longest part of small intestine


mostly locate in pubic and inguinal region


also has plicae circularis, but shorter and less abundant than in jej.


peyers patches, characteristic of ileum, clusters of lymphatic nodules seen on side of ileum opposite to mesentery (picture of intestine with white bump thingys)




absorption of b12 occur here


if removed ileum: pt suffer b12 defic and need injections

2 types of movements in small intestine

segmentations


peristaltic waves






segmentations: contractions of SM that move chyme in both directions


allows greater mixing of chyme with secretions of stomach and intestines




peristalsis: begins in duodenum


these waves overlap, called migrating myoelectric complex (mmc) which is a kind of peristalsis which pushes the chyme forward

ileocecal sphincter or valve

end of small intestine


normally closed


connect small intestine end of ileum to beginning or large intestine at ascending colon (right side) and extends in the cecum




food filing stomach stimulates gastroileal reflex that is increasing peristalsis and opens the ileocecal valve allowing passage from small int to large int



large intestine

include cecum with appendix


(starting on right side)


ascending colon


transverse colon


descending colon


sigmoid colon (little dip after went down descending)


rectum


anal canal




absorbs remaining water, compacts feces and houses symbiotic bacteria!

cecum

blind pouch in right lower abdominal quadrant

vermiform appendix

small blind tubule opening into cecum


removal doesn't affect health of person

hepatic flexure

aka right colic flexure


the 90 degr turn from ascending colon to transverse colon (right side) near the right lobe of liver

splenic flexure

aka left colic flexure


transverse colon turn down to descending colon on left side

anal canal has two sphincters

internal sphincter (made of SM) involuntary




external sphincter (made of skeletal muscle) under voluntary control

muscularis of large intestine

different from other parts of alimentary canal, instead of a longitudinal external layer, muscularis forms teniae coli

teniae coli

3 separate longitudinal ribbons of SM on outside of ascend,transv, desc, sigm colon


(it's the 3 discontinuous bands of longitudinal smooth muscle on exterior)




tenia coli shorter than the intestine so colon becomes sacked btwn teniae forming haustra

haustra

small pouches caused by the sacculations of colon between teniae.


give colon its segmented appearance!

epiploic appendages

small pouches of peritoneum filled with fat and situated along colon and upper part of rectum

the 3 features differentiating large instestine from small instestine

large instestine has


teniae coli


haustra


epiploic appendages

colon motility

haustral churning most of time haustra relaxed and distended, when distension reaches certain point, smooth musc in haustral wall contract and squeeze contents into next haustra


peristalsis moves chyme along ascending colon


mass movements more characteristic for transverse and descending parts, strong contractions 3-4 x/day propel contents towards end of colon

defecation reflex

triggered by distension of rectum




parasymp stim of lower colon and rectum contractions simultaneously with the relaxation of internal anal sphinct

IBD


inflammatory bowel disease

severe chronic and persistent colitis (inflamm of colon)




2 types of IBD:


chron's disease


ulcerative colitis

ulcerative colitis

inflammation of colon mucosa


involves rectum and is continuous without skips




disease confined to cololn


thin bowel wall (mucosa)


disease is continuous (rectum)


ulcers do not cross muscularis mucosae


granulomas uncommon

crohns disease

autoimmune inflamm degeneration of mucosa and underlying layers


severe cases: gut wall perforated and caue fistulas (connect gut with abdominal cavity or outside of body)


intestinal wall becomes thicker and may obstruct lumen


can affect any part of intestine but most common in distal ileum and proximal colon


almost never involves rectum, but can be in anus




lesions found anywhere between mouth and anus


thickened bowel wall with cobblestone appearance


disease occurs in patches: skip lesions


deep ulcers that do cross muscularis mucosae


granulomas common




involves all 4 layers!

colon cancer

second leading cause of cancer related deaths in US


risk fx's: IBD, low fiber diet, increasing age, family hx, polyps


screening is important


two major screening methods: stool occult blood test and colonoscopy

stool occult blood test

quick, cheap, nonspecific test for presence of trace blood in stool


if positive go to more specific diagnoses via colonoscopy and biopsy

colonscopy

visual examination of colon with endoscope

colectomy

colostomy


bowel resection




surgery to remove all or part of large bowel and ileum




removal of entire colon and rectum=proctocolectomy or total colectomy


remove part: subtotal colectomy

diverticulsosis

out pouching of mucosa due to herniation of mucosa

celiac artery (trunk) supplies

foregut


(esophagus, stomach, duod, liver, gall bladder, pancreas, spleen)

Superior mesenteric artery (SMA) supplies

midgut




SMA starts at lower duod and has two loops


cranial lumb of midgut loop forms jejen, il


caudal limb forms il, cec, appendix, ascending and transverse colon (first 2/3)

Inferior mesenteric artery (IMA) supplies

hindgut




ima cranial end starts at distal 1/3 of transverse colon, desc and sigmoid colon


caudal end: cloacae, rectum, anal canal and urogenital bladder

duodenum blood supply

two sources:


proximal part of duodenum (foregut) receives bile and pancr juice from ampulla of vater, receives blood from celiac trunk via gastroduodenal and superior pancreaticoduodenal arteries




distal part starting from sphincter of oddi and down receives blood from inferior pancreaticoduodenal arteries which receive blood via SMA

superior and inferior pancreaticoduodenal arteries

form anastomoses btwn celiac trunk and SMA that allows collateral circulation if needed

duodenal veins dran to

portal vein


either directly or via splenic and superior mesenteric veins

midgut

jej, il and proximal colon including proximal 2/3 of transverse colon receive blood from SMA that runs within mesentery and gives arterial arcades and vasa recta




branches of SMA are named after guts they supply or direction of flow: jejunal, ileal, ileocolic, right colic, middle colic




blood from all these intestines drain into corresponding veins: superior mesenteric vein and eventually to portal vein

hindgut

arterial supplly of distal transverse, descending and sigmoid colon from IMA


which gives left colic, sigmoid and marginal arteries




marginal artery also receives supply from middle colic and forms anastomosis btwn SMA and iMA




(infer mesent vein returns blood from descending and sigmoid colon to portal vein)

branches of SMA

[IMRII]


inferior PD artery


middle colic artery


right colic artery


ileocolic artery


intestinal (jejenal and ileal branches)

marginal artery

anastamoses between middle colic of SMA and left colic of IMA




common site for ischemia

branches of IMA

[LSS]


left colic artery


sigmoid artery


superior rectal artery



only regions in GI tract that have glands in submucosa

Esophagus (not as abundant as in-->)


Duodenum

esophageal muscularis externa

smooth and skeletal muscles


upper part: skeletal


lower part: smooth fibers


middle: both


(these fibers make the internal circular and external longitudinal layers)

esophagus serosa vs adventitia

esoph inside abdominal cavity: serosa covered




before esoph passes thru diaphragm its: adventitia covered

esophagus characteristics on slide

lumen lined by thick layer of nonkeratin'd stratified squamous epithelium that normally appears as silky offwhite velvety surface


*contain submucosal gland (only other place that also has this..?)



gastro esophegeal jxn

shift from stratified squamous epithelium of esophagus to the simple columnar epithelium of stomach

stomach cells and gastric pit

stomachs rugae are thick folds of mucosa and submucosa




internal surface lined with simple columnar epithl and goblet cells




invaginations of epithel into mucose are gastric pits/foveolae:




regenerative cells (mostly at isthmus, top of pit, top of neck)


they divide to replace other cells in gastric glands






pareital (oxyntic cells) mostly at neck of pit which is middle way down pit) make HCl and IF




cheif cells (zymogenic cells, at base of pit) make pepsinogen and gastric lipase




enteroendocrine cells present in most of gi tract make hormones.


in stomach make gastrin and histamine




g cells make gastrin




mucus neck cells produce mucus and bicarbonate, protect stomach epithel from damage by stomach acid. they appear pale and contain obvious mucous droplets

if i see glands in the mucosa*

its the stomach.

small intenstine

most distinctive ft.: large SA


bc of plicae circularis (valvs of kerckring, circular folds) permanent transverse folds involving submucosa


the actual big fold




epithel: simple columnar




villi: finger like protrusions of lamina propria


the little folds off the big fold




core of villus




lacteals (lymphatic capillaries) central lymphatic vessel in core of villus (extension of lamina propria (so like opposite of what the folds are cuz its in the middle of fold)


crucial for absorption of lipids


on slide it looks like white area within fold




look at the pic cuz its like big folds and then the little folds along the big fold


the little folds are villi


its a curvy fold







duodenum

has brunners glands in submucosa (other sections dont)




villi in duod are taller, fatter, broader than in other sections

jejenum

NO brunners gland in submucosa


NO peyers patces in lamina propria




means its jejenum




well dvlpd villi more narrow and sparse than in duod






and remember,


less complex arterial arcades


longer vasa recta


more plicae circularis, thicker, more highly folded


no fat in mesentery

ileum

has peyers patches lamina propria




villi in the ileum are shortest and narrowest




and remember,


more complex arterial arcades


shorter vasa recta


less plicae circularis, thinner, less folded


fat present in mesentery



colon (large intest) histology

surface looks even across


crypts all the way down


nothing in submucosa


no vili


goblet cells in epithelium




instead of outer longitudinal layer there are teniae coli, the 3 bands

barretts esophagus

weakness of LES so acid from stomach spill up into esophagus




charact'd by replacement of stratified squamous epithelium (normal esoph epithel) with columnar epithelium with goblet cells (gastric mucosa)




presence of goblet cells is most significant criteria for dx of barretts

aplasia

failure to dvlp


something didnt grow in baby

heteroplasia

growth of normal tissue in wrong place

metaplasia


low grade dysplasia

metaplasis, low grade dysplasia


abnormal transformation of an adult fully differentiated tissue of one kind into differentiated tissue of another kind


highly diff replace by highly diff




ie barretts esophagus



dysplasia


aka hi grade dysplasia

hi grade dysplasia


abnormal transformation of highly diff'd into lowly diff'd tissue


cells become smaller, nuclei more active, more heterochromatin (char of lowly diff)


precancerous condition

adenoma

benign gland like looking tumor

adenocarcinoma

malignant tumor that looks similar to a gland


its an adenoma turned cancerous

lowly differentiated cancer cells

high nucleus to cytoplasm ratio


more nucleus than cytoplasm


heterochromatin rich nuclei that are BIG


lots of mitotic figures




see dark inside nucleus of cell so darkness taking up most area of cell.