GI Summy 1

intraperitoneal organs

floppy and suspended by mesentery

retroperitoneal organs

adhered to the back wall

Foregut

esophagus → stomach → proximal half of duodenum → liver → gallbladder → pancreas

stomach

intraperitoneal

duodenum

intraperitoneal

liver

intraperitoneal

gallbladder

intraperitoneal

pancreas

retroperitoneal

Midgut

distal half of duodenum → jejunum → ileum → cecum → appendix → ascending colon → 2/3 of the transverse colon

jejunum

retroperitoneal

ileum

retroperitoneal

cecum

intraperitoneal

ascending colon

retroperitoneal

transverse colon

intraperitoneal

Hindgut

distal 1/3 of transverse colon → descending colon → sigmoid colon → rectum → anal canal

descending colon

retroperitoneal

sigmoid colon

intraperitoneal

rectum

retroperitoneal

3 features of the gut barrier and how they help to prevent inflammation and infection

1. mucus layer → forms a physical barrier to weep and sweep pathogens/toxins/etc → get excreted out

2. epithelium → physical layer that also produces varies mucins, antimicrobial peptides (defensins), etc

   • also transport igas which are produced in the submucosa

3. submucosa → production of igas which released in secretions like breast milk and into gut

pain in gi system

sensed by nerves of the GI

ENS has both sensory and motor nerves → chemoreceptors and baroreceptors that sense mechanical stretch

pain can be stimulated via three mechanisms

1. mechanical stretch stimulus, eg peristalsis issue or obstruction of the lumen (tumor)

2. direct chemical activation via PGs, histamine, inflammatory mediators, acid, K+ etc

3. inflammatory processes eg mast cells

any of these processes can stimulate a neuron → synapse onto an interneuron → sends signal to spinal cord = pain

gi motility

segmentation → mixing and churning that enhances digestion

peristalsis

tonic contraction → prevents backflow across sphincter

PANS GI Motility

rest and digest

affects smooth muscle contraction and plays a role in peristalsis via M3

SANS GI Motility

inhibit smooth muscle contraction via beta 2 and alpha 2

ne decrease amplitude of slow depols

ileus

decreased or absent contractions in the small intestine

gastroparesis

muscles in the stomach don't move food as they should for it to be digested

bulk-forming laxative onset

12-24 hours, may take up to 72 hours

daily fiber recommendation

38 g for men

25 g for women

stool softener onset

1-3 days

stimulant laxative onset

6-8 hours PO

saline laxative onset

1-3 hours

peg onset

17-72 hours

loperamide bbw

fatal arrythmias

t cell response to infection

infection → antigen delivered to lymphoid organ → naive T cell encounters antigen → T cell activation → proliferation → differentiation into effector cell → elimination of infection

t reg

can sense “harmless” antigens → generate immunosuppressive cells to suppress other T cells which could drive autoimmunity

release suppressive cytokines and sequester growth factors to prevent stimulation

peyers patch

where immune cells congregate in both the large and small intestine

most likely found in ileum

short term steroid effects

- increased glucose

- high bp

- increased appetite

- stomach upset

- mood changes (euphoria)

- insomnia

long-term steroid effects

- infection

- hair loss

- glucose intolerance

- moon face

- weight gain

- myopathy

- steroid induced diabetes

- osteoporosis and glaucoma

azathioprine bbw

lymphoma when used in conjuction with infliximab

azathioprine monitoring

- 6MMP for toxicity
- 6-TGN for efficacy

methotrexate bbw

- BBW -> issues with bone marrow, hypersensitivty, etc
- teratogenic

infliximab bbw

risk of severe infection, lymphoma in conjuction with aza

infliximab onset

6 weeks or more

vedolizumab

binds integrin and interferes with T cell migration to gi tract

slower onset

risankizumab

block T cell differentiation

when to use risan and vedo?

when pt fails inflix

upadacitinib

block transrciption and translation of cytokine releasing genes

fastest onset of 2 weeks

upadacitinib bbw

cancer, serious infection, CV events, thrombosis

penetrative dx for crohns

fistulas, abscesses, stricture

fluid absorption

occur via villi

na absorption will stimulate fluid reabsorption

driven by na/k atpase just like in kidneys

na/h antiporter regulated bt ATII

steroids stimulate na/k atpase and increase ENaC channel expression

E will affect na/k atpase

fluid secretion

occurs via crypts

stimulation of cl channels stimulates water secretion

histamine/5-ht from mast cells will stimulate ens and cl channels

chronic inflammatory diarrhea

blood in stool

secretory chronic diarrhea

• does not improve with fasting

• issue with malnutrition (flushing out everything you eat so fast), or GI protein loss

• theres an active secretion of electrolytes → some activation of cl channels by smth

osmotic chronic diarrhea

• stops with fasting

  • diet is an effective treatment for this subtype, eg lactose intolerance

• some nonabsorbed, osmotically active substance present in the gut

fatty chronic diarrhea

• improper digestion of fat due to lack of bile acids

  • think of issues with your hepatobiliary system (liver, gallbladder, pancreas)

• may also have poor malabsorption

  • some structural abnormality or damage to epithelium preventing fat absorption

functional chronic diarrhea

• may be associated with increased permeability of the gut

  • function due to lack of significant change in gut structure

when to refer pt to dr for diarrhea?

no improvement after 48 hr

when to refer pt to dr for constipation?

s/sx dont improve after week

vomit reflex gi

any injurious stimuli from gi releases 5-ht and dopamine

vomit reflex vestibular

• vestibular system helps coordinate walking w/your head and eyes so you know where you are in space

  • mismatch between visual input can trigger reflex

  • releases ach and histamine

vomit reflex ctz

• ctz is part of the vestibular system, allows body to sample blood and csf for toxins

  • releases 5-ht and dopamine

which meds cause qtc prolongation?

phenothiazine derivatives for n/v

serotonin blockers for n/v and ibs-d

d2 antagonist for n/v

tca for ibs pain

alosetron bbw

ischemic colitis

lack of perfusion to gut damaging colon

eluxadoline

• may cause pancreatitis, pts with gallbladder removal at higher risk of this se

  • so are pts who drink a ton

plecanatide bbw

dehydration in kids younger than 6

tenapanor bbw

dehydration in kids younger than 6