GI

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cholecystitis

recurrent episodes of RUQ or mid-upper pain

Peptic ulcers (PUD) : gastric vs. duodenal ulcers

Gastric - worse with eating, more episodic
- H. pylori
Duodenal - worse 2-3 hrs after eating, may awaken during night, more continuous pain

Intestinal atresias: duodenal and jejunal/ileal atresias

Intestinal atresias - both pres in 1st 1-2 days of life

Duodenal atresia - doesn't recanalize
- "double bubble" on imaging
- associated w Down syndrome

Jejunal/ileal atresia - disruption of mesenteric arts => necrosis => bowel discontinuity
- segmental resorption
- "apple peel" on CT w contrast

Gastrin

From G cells (stomach antrum)
- inc gastric H+ secretion (also by inc gastric mucosal growth)
- inc gastric motility


Inc release if stomach is distended, basic or *Vagal N. stim via GRP (Gastrin-releasing peptide)
- also inc in H. pylori gastritis
- BIG inc in Zollinger-Ellison syndrome - from gastrinoma

Somatostatin

Somatostatin - from D cells (in GI mucosa, pancreatic islets)
- dec gastric acid AND pepsinogen = dec overall small intestine and pancreatic fluid secretion
- dec gallbladder contraction
- *dec insulin AND glucagon


SST inc if acidic, and dec if Vagal N. stim


*Blocks secretion of several hormones

Drugs: Ocreotide - SST analog to trx acromegaly, carcinoid syndrome, bleeding esophageal varices

Cholecystokinin

CCK = from I cells (in duodenum and jejunum)
- *promotes emptying of gallbladder (inc gallbladder contraction and sphincter of Oddi relaxation)
- inc pancreatic secretions - bc emptying gallbladder => also want to inc pancreatic secretions to digest more ? (via Muscarinic pathways)
- dec gastric emptying to allow GB to empty 1st


CCK inc with fatty acids and aas (protein, basically w food)

Secretin

Secretin = from S cells (in duodenum)
- *works totally in duodenum
- inc pancreatic HCO3- secretion! and dec gastric acid => **so that bicarb can neutralize gastric acid in duodenum => so pancreatic enzymes can be activated and digest
- also inc bile secretion - to work with pancreatic enzyme digestion, and get released at same time after eating!


Secretin inc if acidic environment => to balance it
- inc when eat fatty acids

Glucose-dependent insulinotropic peptide = Gastric-inhibitory peptide (GIP)

GIP = from K cells (in duodenum & jejunum)
- Exocrine: dec gastric H+
- **Endocrine: inc insulin = link b/w eating => and insulin inc


GIP is inc w eating
- *so insulin inc w eating glucose (vs. doesn't with IV glucose) bc of GIP in GI tract

Motilin

Motilin = in small intestine
- makes migrating motor complexes (MMCs) = inc peristalsis when FASTING (b/w meals)


Motilin receptor AGonists (Erythromycin) => inc peristalsis

Vasoactive intestinal polypeptide (VIP)

VIP = in **parasymp ganglia in sphincters, GB, small intestine
- **net = vasodilator to dec BP (?)...
- by inc water and electrolyte secretion from GI tract! => more watery stool
- by relaxing GI smooth muscle and sphincters


VIP inc with any abd distension (want to lose fluid) and Vagal N. stim (Vagal N. stim inc digestion) (Gastrin has same triggers to inc it)
BUT dec w Adrenergic inputs (which are symp)


VIPoma = non-Alpha, non-Beta islet cell pancreatic tumor secreting VIP
- causes: *watery diarrhea, hypokalemia (bc fluid secretion), achlorhydria (no gastric acid) why?????

Nitrix Oxide (NO)

NO - inc smooth muscle relaxation!
- so also relaxes LES (lower esophageal sphincter)


...so loss of NO secretion => dec LES tone = achalasia


Achalasia - can't push food out bc LES canNOT relax (failure of esophageal peristalsis too?)

Ghrelin

Ghrelin = in stomach
***appetite stimulant!!! = HUNGRY
- so obvi inc w fasting and dec w food


High Ghrelin in Prader-Willi syndrome (constantly hungry, genetic)
Dec Ghrelin post-gastric bypass surg (less stomach tissue to secrete Ghrelin)

Intrinsic factor (IF)

IF = in Parietal cells (of stomach)
*acts as Vitamin B12-binding protein in terminal ileum = NEEDED for B12 uptake!


X Parietal cells or IF => B12 deficiency
- autoimmune destruction of parietal cells w Chronic gastritis and Pernicious Anemia

Gastric acid

Gastric acid = secreted by Parietal cells (in stomach)
*dec stomach pH => more acidic for digestion


Inc acid by Histamines, Vagal N. stim (ACh), Gastrin
Dec acid by SST, GIP, Prostaglandins, Secretin

Pepsin

Pepsin = from Chief cells (in stomach)
*for PROTEIN digestion


Pepsin is inc by Vagal N. stim (ACh) or local acid
- *Pepsinogen => Pepsin in presence of H+ (so if there's more local acid H+, converts more Pepsinogen to Pepsin)

Bicarbonate (HCO3-)

Bicarb = secreted from mucosal cells (in stomach, duodenum, salivary glands, pancreas) AND Brunner glands in duodenum
- so duodenum releases lots of Bicarb?
- to neutralize acid => inc pH towards basic


*Secretin inc HCO3- bc Secretin inc pancreatic and GB secretion => so also inc pH to basic so that pancreatic enzymes can be activated to work and digest

Portal Triad

Portal Triad
1. Proper Hepatic Artery
2. Portal Vein
3. Common Bile Duct

Retroperitoneal structures

Retroperitoneal structures: SADPUCKER
Suprarenal (adrenal) glands
Aorta & IVC
Duodenum (2nd, 4th parts)
Pancreas
Ureters
Colon (Asc & Desc limbs)
Kidneys
Esophagus
Rectum

Hypertrophic pyloric stenosis

Hypertrophic pyloric stenosis = most common cause of gastric outlet obstruction


Pres: nonbilious projectile vom at 2-6 wks old, visible peristaltic waves, olive-shaped mass palpable in epigastric region
- esp firstborn males, when exposed to Macrolides abx
- result: hypochloremic metabolic alkalosis (from vom and volume contraction)
- US w thick, long pylorus
Trx: pyloromyotomy