GI System

Anatomy

Upper GIT

Oral Cavity

soft palate

covered by palatine apopneurosis

hard palate

palatine process of maxilla, palatine bone, hamulus of sphenoid bone

mucosa over it
anterior part is rough = rugae to hold fold
posterior part is smooth

muscles of the oral cavity floor

  • myohyoid
  • geniohyoid
    both can alter the position of the hypoid, and thus pulls the attached larynx

Muscles:
palatoglossus
palatopharyngeus
together, they depress the soft palate to close off the oral cavity
tensor veli palatini = tenses soft palate
levator veli palatini = elevate soft palate
musculus uvula

vestibule

  • opposite upper 2nd molar is the opening of duct of parotid gland

Tongue

extrinsic muscles: 🚩

  • hyoglossus = depress
  • genioglossus = pull tongue forward
  • palatoglossus = elevate
  • styloglossus = pull tongue backward

intrinsic muscles of the tongue:

  • superior longitudinal
  • tranverse and vertical
  • inferior lonigitudinal
    changes shape of the tongue

papilla:

  • circumvalate = just anterior to the terminal sulcus
  • filiform = more central
  • fungiform = more lateral
    all except filiform have sensory taste buds
    in pharyngeal part, there are many lingual tonsils

terminal sulcus = separates anterior (oral) part and posterior (pharyngeal) part
V-shaped, in the middle is foramen caecum

Frenulum = mucosa from base of oral cavity to the inferior side of tongue
at the base on both sides are sublingual caruncle
beside the frenulum are deep lingual veins - visible

Salivary glands

Parotid

covered by a fibrous capsule, prevents expansion

structures that runs in it: 🚩:

  • facial nerve
  • external carotid artery
  • retromandibular vein

auricotemporal nerve runs between parotid and the auricle

  • supplies the parotid fascia, TMJ, skin over temporal area, auricle, external acoustic meatus
  • when the parotid gland swells and expands, it stretches the fascia and compresses the nerve = causes pain in the regions it innervates

duct pierces over the buccinator muscle, opens opposite the upper 2nd molar teeth into vestibule

Sublingual gland

secrete serous

secrete mucous

have short ducts that directly open into the sublingual fold into the oral cavity

Submandibular gland

secrete mucous + serous

have a very long duct = common site of stone

  • duct goes from the deep portion and opens into the sublingual caruncle

gland has deep and superficial portion

treatments to salivary stone:

  • give acidic to increase secretion to push the stone out, painful so give anaesthetic
  • ultrasound
  • surgery (invasive)

Pharynx

pharyngeal wall

  • mucous membrane
  • pharyngobasilar fascia
  • muscle: inner levator, outer constrictor
  • buccopharyngeal fascia

constrictors

  • superior
  • middle
  • inferior => thyropharyngeal and cricopharyngeal

pharyngeal diverticulum = bulging of the wall in area of muscle weakness (in between thyropharyngeus and cricopharyngeaus)

levators:

  • stylopharyngeus
  • palatopharyngeus
  • salpinopharyngeus

verrucae = infront of epiglottis
piriform fossa = behind epiglottis

Oesophagus

upper sphincter = cricopharyngeal part of inferior constrictor muscle
lower sphincter = formed by right crus of diaphragm

constrictions:

  • arch of aorta 22cm
  • left main bronchus 27cm
  • right crus of diaphragm 38cm

start at C6 (where cricoid cartilage ends)
pierces diaphragm at T10

muscle

  • upper 1/3 is striated, rest is smooth

Lower GIT

Peritoneum

greater omentum

  • from the greater curvature of stomach to the bottom, then go back up to attach to transverse colon, then go to posterior wall
  • goes in front of small intestine
  • 4 layers
    (gastrocolic omentum only has 2)

lesser omentum

  • from the lesser curvature of stomach to the liver
  • 2 parts: hepatogastric and hepatoduodenal
  • right free margin of lesser omentum forms the epiploic foramen

divided into quadrants and regions

regions:

  • divided by midclavicular lines vertically and subcostal and transtubercular plane horizontally

greater sac

  • divided into supracolic and infracolic by the transverse mesocolon
  • infracolic further divided into left and right by the mesentery of small intestine
  • supracolic and infracolic communicate via the left and right paracolic gutter

lesser sac

  • area behind the stomach and liver
  • give potential space of stomach to expand
  • left limit formed by splenorenal ligament and gastrosplenic ligament
  • access to lesser sac is through the omental foramen, cut through transverse mesocolon, gastrocolic omentum, hepatogastric ligament

retroperitoneal structures:

  • pancreas (except tail)
  • 2+3 duodenum
  • A+D colon
  • kidney

stomach

opening:

  • gastro-oesophageal (cardia)
  • pyloric orifice

stomach bed:

  • left kidney
  • left ureter
  • spleen
  • neck, body, tail of pancreas

nerve innervation = T6-T9 sympathetic, referred pain to epigastric region and subcostal

hiatus hernia formed by the weakening of right crus of diaphragm

GUT

Foregut

lower oesophagus, stomach, to upper 1/2 of descending (2) duodenum (major duodenal papilla)

supplied by celiac trunk

nerve: T6-T9 sympathetic

Midgut

lower 1/2 of 2nd part duodenum to the proximal 2/3 of transverse colon

supplied by superior mesenteric artery

nerve: T10-T12

Hindgut

distal 2/3 of TC to upper rectum

supplied by inferior mesenteric artery

nerve L1-L2

Small intestine

Duodenum

1st = superior
2nd = descending
3rd = transverse
4th = ascending

only 2nd and 3rd are retroperitoneal

C-shaped in the L2 vertebral region, where pancreas lies

major duodenal papilla at the postero-medial aspect of middle of descending duodenum

only the first 2.5cm don't have plicae circulares, rest do

DJ flexure is intraperitoneal

Jejunum

has the most plicae circulares

have long vasa recta with few arterial arcade

wider c.f. ileum

ileum

has least/no plicae circulares

short vasa recta, many arterial arcade

narrower lumen c.f. ileum

have peyer's patches = lymphoid aggregates

have Brunner's glands = secrete alkaline fluid and mucous

more fat in mesentery c.f. jejunum

histological features of small intestine:

  • villi
  • microvilli
  • intestinal glands

Large intestine

histological features:

  • simple tubular glands
  • plasma cells
  • epithelium has lots of absorptive cells (enterocytes) and goblet cells

gross features:

  • plicae circulares (thickened bands of longitudinal smooth muscle)
  • haustra pouches
  • appendices epiploica
  • appendix (can be in retrocaecal, subcaecal, pelvic, pre-iliac, post-iliac)

only transverse is intraperitoneal = transverse mesocolon

Rectum = transverse rectal folds to short faces and allow air through

Cases

Peptic Ulcer

mainly in duodenum
also in antrum of stomach

imbalance of protective factors and aggressive factors, leading to damage to mucosa
protective: mucous, HCO3, prostaglandin E2
aggressive factor: HCl, enzymes (pepsin), NSAIDs, H. pylori, smoking (impairs blood flow

H pylori

  • Gram negative non-sporing rod bacteria
  • causes peptil ulcer in the stomach antrum
  • lives in the surface mucous layer = does NOT invade epithelium
    causes peptic ulcer by:
  • producing urease, which converts urea into CO2 and NH3, increasing pH so making the environment hospitalizable
  • immune response (T and B cell activaton) and intense inflammation, leading to release of interleukin from epithelial cells, which recruit and activate neutrophils
  • increases gastrin production => increases acid secretion
  • produces phospholipase which assist in mucous breakdown
  • produce Cag A gene, wrhich regulates production of vaculating toxin causing epithelial damage
    all leads to damage to epithelial, causing leakage of nutrients and sustenance of bacteria

pathological features: ⭐

  • red inflammation of mucosa = gastritis
  • smooth and clean base
  • punched out, straight wall
  • fibrotic contractions causes rugae folds coming out from central ulcer

histological features: ⭐

  • 4 layers: dnecrotic base, inflammation, granulation (vascular and fibrotic), fibrosis
  • thinning of wall at the base of ulcer
  • loss of muscle cell

treatment:
omeprazole = PPI to treat the gastritis, prevent further acid secretion
combination of antibiotics to kill H pylori

  • amoxicillin
  • clarithromycin
  • metaprozole

complications:

  • haemorrhage (ulcer hits a blood vessel)
  • perforation of the wall
  • penetration into adjacent organ

IBS

Ulcerative Colitis

Crohn's disease

involves CD4 TH2 immune response

gross pathology:

  • reddened inflammed mucosa
  • broad base ulcers with regenerating epithelium bulging into lumen, forming pseudopolyp

affects mainly rectum, then continue proximally, even reaching terminal ileum

histology:

  • affects the mucosa only
  • regenerating epithelium
  • ulceration leading to inflammation
  • crypt abscess= acute inflammatory exudate (abscess) in the crypt => decreased no. of goblet cells

complications:

  • toxic colon = due to severe inflammation where the mediators have caused neuromuscular dysfunction, with decrease in tone of SMC and loss of peristalsis, bowel dilates
  • development of dysplasia
  • haemorrhage

involves CD4 TH1 immune response

affects all of GIT, separated by normal mucosa = skip lesions

gross pathology:

  • serpentine linear ulcers, and normal mucosa intervening, forming a cobblestone appearance

histology:

  • thickening of wall due to fibrosis, fibrotic contractures causes narrowing of lumen, forming a stricture
  • transmural inflammation
  • fissure = deep ulceration and inflammation that extends down into the mesentery
  • fistula = abnormal communication between 2 adjacent organs
  • granulomatous formation = contains epitheloid cells, giant cells, amcropahges, lymphocytes but NO necrosis, occured due to Th1

complication: increased risk of carcinoma, fistula

treatment:
aminosalicylic acid = for mild-moderate IBD (anti-I)
glucocorticoid = symptom relief (anti-I)
immunomodulators = inhibit DNA synthesis of immune cells (only for CD)
antibodies = inhibit TNF
antibiotics

Colorectal cancer

2 pathways:

adenoma carcinoma sequence (APC-beta-catenine) = mutation in the APC- beta catenine gene that leads to loss of function of tumour suppressor genes
can change from benign lesion into polyp and as mutation accumulates, growth is less regulated and malignancy develops

mismatch repair gene = mutation in any of the 5 mismatch repair gene that causes microsatellite instability

adenomatous polyp can be:

  • sessile = raised, flat lesions
  • serrated = glandular, with a stalk

dysplasia

low grade:

  • abundant mitosis
  • high N:C ratio
  • nuclear pleomorphism
  • nuclear moulding
  • decreased goblet cells
  • nuclear polarity normal
  • architecture is normal

high grade dysplasia:

  • architecture is changed
  • loss of nuclear polarity

carcinoma in situ: dysplastic but no invasion of basement membrane

invasion

left side lesion = causes obstruction

  • narrowing of lumen
  • changes in bowel habit

right side lesion = anaemia

  • larger lumen so dilation
  • anaemia => dark stools, mainly liquid

desmosplastic stroma :flag:
fibrovascular tissue that supports the tumour
produced due to cytokines produced by the tumour cells
suppply blood and nutrents
as it is fibrous tissue, can contract and causes thickening of bowel wall and narrowing of lumen, predominant in left side lesion

spread:

  • via lymph nodes
  • haematogenous (rare but most severe)
  • invasion into adjacent structures/organs
  • via serosal surface into peritoneal cavity

TNM staging system:
Tumour:
Tis = carcinoma in situ
T1 = into submucosa
T2 = into muscularis externa
T3 = into serosa
T4 = into adjacent tissue


Node
N1 = 1-3
N2 = 4 or more


M1 = metastasis

Jaundice

prehepatic = haemolytic or Gilbert's syndrome

increased urobilinogen
increased unconjugated bilirubin
increased AST
normal ALT
reticulocytes
decreased Hb

intracellular acute = hepatitis

increased conjugated bilirubin
increased urine bilirubin
normal serum albumin
very high ALT and AST
may have high GGT and ALP

intracellular chronic = cirrhosis

increased conjugated bilirubin
decreased albumin
high ALT and AST
increased urine bilirubin
increased PT time
no response to vitamin K
decreased plasma cholesterol

extrahepatic cholestasis

increased conjugated bilirubin
very high GGT and ALP
increased urine bilirubin
decreased urine urobilinogen
increased PT time
response to vitamin K
high plasma cholesterol (due to failure to excrete bile)

dark yellow urine = high urine bilirubin

pale stool = low urine urobilinogen

medically unexplained syndrome (e.g. IBS)

no diagnosis found yet
false negative
somatosization
low sensitivity/specificity test

Infectious gastroenteritis

bacteria = Campylobacter jejuni
viral = rotavirus

causes inflammatory diarrhoea

becomes hypokaelemic and metabolic acidotic

antibiotic associated diarrhoea = Clostridium difficile

complications: ⭐:

  • Guillian Barre syndome
  • reactive arthiritis
  • bacteremia
  • IBS