GI

4 common complaints/ S+S for GI disease?

1) abdominal or chest pain

2) altered indigestion of food from N/V, odyno/dysphasia

3) Altered bowel movements

4) GI bleeds

what must you consider when tx a patient with any GI condition S+S?

all cases of GI pain present differently - patient dependent

what will a upper vs lower GI bleed show via stool?

upper - melena (black tarry stool)

Lower- hematachezia (bright/frank red blood)

what is considered upper GI vs lower GI ?

upper- duodenum and up

lower- below the duodenum

How can a primary GI disease cause vitamin deficiencies?

GI disease → Malabsorption (poor nutrient absorption) → Vitamin deficiencies → Systemic symptoms.

acute complications of GI disease ?

dehydration, sepsis, bleeding, shock

Chronic Complications of GI Disease?

malabsorption and deficiency states

what is GI tract disease partial or complete blockage caused by?

adhesions and stenosis due to the connective tissue coming together in response to inflammation

What are the 4 layers of the GI tract wall (from lumen outward)?

**Mucosa - Innermost epithelial lining; contains glands.

Submucosa - Connective tissue.

Muscularis externa - Muscle layer responsible for movement.

Serosa - Outermost protective covering.

Mnemonic: My Stomach Makes Sounds (MSMS).

Mucosa 3 components?

epithelium, lamina propria*, muscularis mucosae

what is the lamina propria ?

Loose connective tissue beneath the epithelium in the GI mucosa; contains blood vessels, lymphatics, and immune cells.

just know binds the epithelial cells together

What is the submucosa of the GI tract?

Loose connective tissue directly beneath the mucosa.

Contains larger blood and lymphatic vessels.

Contains Meissner's (submucosal) nerve plexus, part of the enteric nervous system.

Meissner's plexus controls GI secretion.*

What is the muscularis externa of the GI tract?

Inner circular and outer longitudinal layers of smooth muscle.

Responsible for GI motility (peristalsis).

Contains Auerbach's (myenteric) plexus between the two muscle layers.

Auerbach's plexus regulates GI motility.*

Meissner vs Auerbach

Meissner = Secretion (submucosa)

Auerbach = Motility (muscularis externa)

secretions of the GI tract

salivary, gastric, pancreatic, biliary, intestinal 7 L secretions a day

(bs)

what is GI motility

Coordinated smooth muscle contractions that move and mix secretions and luminal contents from mouth to anus.

What is GI absorption?

The process of taking digested nutrients into the body:

Amino acids

Small peptides

Monosaccharides

Fatty acids

How do nutrients cross the intestinal epithelium during absorption?

Transcellular: Through epithelial cells.

Paracellular: Between epithelial cells.

Nutrients enter the blood or lymphatic system.

(superior and inferior mesentery) Intestinal venous blood → Portal vein → Liver= absorption

How does the GI tract provide defense?

The GI mucosa acts as a protective barrier against the external environment, including ingested bacteria and toxins.

How can GI fluid imbalance cause diarrhea?

↑ Secretion OR ↓ Absorption → Diarrhea.

Can be fatal due to excessive fluid and electrolyte loss.

What does the GI tract excrete?

Undigested food products

Bacteria

Certain heavy metals (copper and iron, excreted in bile)

excreted via feces

How does the GI tract regulate fluid and electrolyte balance?

Small intestine receives 8-9 L of fluid with electrolytes/day.

Secretes an additional 1 L/day.

MORAL OF THE STORY= Secretion and absorption must be balanced

Where are GI hormones secreted from?

Endocrine cells scattered throughout the mucosa of the stomach and intestine, rather than concentrated in specialized glands.

What are the functions of GI hormones?

Have dual functions as hormones and neurotransmitters.

Many GI hormone levels increase after feeding.

hormone charts on pg 31 +32

31-32

What does gastrin do, and what disease is associated with it?

Stimulates gastric acid secretion.

Zollinger-Ellison syndrome → Excess gastrin → Excess stomach acid → Peptic ulcers.

What does CCK do?

Stimulates gallbladder contraction → Releases bile.

Stimulates pancreatic enzyme and bicarbonate secretion.

What do GIP and GLP-1 do?

GIP: Stimulates insulin release and inhibits gastric acid secretion.

GLP-1: Stimulates insulin secretion → Lowers blood glucose.

Both are incretin hormones.

GLP-1 do what ?

↓ Gastric motility/emptying → ↑ Satiety (fullness)

What is intrinsic factor, and what happens if it's deficient?

Secreted by gastric parietal cells.

Binds vitamin B12 to facilitate absorption.

Autoimmune destruction of parietal cells → ↓ Intrinsic factor → ↓ B12 absorption → Pernicious anemia.

histamine and leptin

Histamine: Needed for GI secretion.

Leptin: Decreases appetite.

Prostaglandins?

Protect gastric mucosa; NSAIDs reduce this protection → Ulcers.

What is paracrine control?

Local cell signaling in which substances act on neighboring cells. They have a short half-life because they are rapidly removed or degraded.

paracrine vs endocrine

Endocrine = Travels through blood to distant cells.

Paracrine = Acts on nearby cells.

What are examples of paracrine signaling in the GI tract?

Histamine: Stimulates gastric acid secretion.

Somatostatin: Inhibits gastric acid secretion.

Serotonin (5-HT): Released in the small intestine to regulate vagus nerve activity.

what do the different regions of the stomach mucosa secrete?

Cardiac: Mucus

Fundic: Mucus, acid, pepsin

Pyloric: Mucus

(Pepsinogen is secreted first and converted to pepsin by stomach acid.)

How does destruction of parietal cells cause pernicious anemia?

Parietal cell destruction → ↓ Intrinsic factor → ↓ Vitamin B12 absorption → B12 deficiency → Megaloblastic anemia (pernicious anemia).

What are the 3 main stimulants of gastric HCl secretion?

Acetylcholine (ACh)

Gastrin

Histamine

All three stimulate parietal cells → ↑ HCl (stomach acid) secretion.

Where do the 3 main stimulants of gastric acid secretion come from?

Acetylcholine: Released by vagal postganglionic and enteric neurons during feeding. (eat to stimulate vagal cells)

Gastrin: Released by G cells in the gastric antrum.

Histamine: Released by ECL and mast cells; binds H2 receptors.

What happens when excess gastrin is produced by a tumor?

↑ Gastric gland and parietal cell growth (hyperproliferation).

↑ Gastric acid secretion.

Can cause Zollinger-Ellison syndrome → Peptic ulcers.

What causes Zollinger-Ellison syndrome?

A gastrinoma produces excess gastrin → excessive gastric acid secretion → recurrent peptic ulcers.

Remember: Zollinger-Ellison = Too much gastrin = Too much acid.

What is the pathophysiology and presentation of Zollinger-Ellison syndrome?

Gastrinoma (tumor) → ↑ Gastrin → ↑↑ Gastric acid secretion → Excess acid enters small intestine.

Causes:

Peptic ulcers: Excess acid damages intestinal mucosa.

Steatorrhea: Low pH inactivates pancreatic lipase → Poor fat digestion → Fatty, oily, floating stools.

Diarrhea: Excess intestinal fluid and impaired absorption.

Why does Zollinger-Ellison cause steatorrhea?

Excess acid → ↓ Intestinal pH → Inactivates pancreatic lipase → Fats aren't properly digested → Steatorrhea (fatty stools).

Zollinger-Ellison key findings ?

Gastrinoma + Excess acid + Ulcers + Diarrhea + Steatorrhea.

presents with ulcers + diarrhea + steatorrhea

too much PPI (end in PROZOL) use leads to?

prolonged high luminal PH --> leads to stimulation of hyper secretion of gastrin stimulating the hyperplasia of histamine-secreting ECL cells

increase PPI to increase X to increase X to X ?

too much PPI leads to increase PH to increase gastrin secretion then hyperplasia of mucosal cells / ECL cells

why is the ECL cell growth bad?

Rebound acid: Can cause heartburn or acid reflux after stopping PPIs.

ECL cell hyperplasia: Long-term gastrin stimulation can cause changes in the gastric mucosa.

ECL cells do what

ECL cells = Enterochromaffin-like cells.

They are cells in the stomach lining that release histamine, which stimulates gastric acid secretion.

Why can stopping long-term PPI treatment cause rebound acid secretion?

Prolonged PPI use → ↓ HCl → ↑ Gastrin → Growth of acid-regulating cells (especially ECL cells).

Stopping PPIs → Acid suppression ends → Rebound ↑ gastric acid secretion.

Symptoms: Heartburn and acid reflux.

Key concept: The stomach temporarily produces more acid than before treatment.

tx of overconsumption of PPIs?

Stop the drug - note the rebound acid produced though because increase content of parietal cells and gastrin secreting cells

How does somatostatin inhibit gastric acid secretion, and where is it released?

Secreted by D cells in the gastric antrum and corpus.

Directly: Inhibits parietal cells → ↓ cAMP → ↓ H⁺ secretion.

Indirectly: Inhibits gastrin and histamine release → ↓ HCl secretion.

Remember: Somatostatin inhibits acid secretion both directly and indirectly.

what are the phases of gastric acid secretion?

cephalic, gastric, intestinal

What is the cephalic phase?

(~30% of response) Is initiated by the sight, smell, taste, and swallowing of food

how does the cephalic phase work?

Stimuli activate the dorsal motor nucleus of the vagus nerve in the medulla.

Activates the vagus nerve (parasympathetic) → ↑ Gastric acid secretion.

Remember: Cephalic phase = Brain senses food → Vagus nerve activated → Stomach prepares for digestion.

What is the gastric phase?

(~70% of response) of secretion is induced by stimuli within the stomach

how does the gastric phase work ?

as soon as bolus enters the stomach + produces distention --> vasovagal reflex --> release ACh --> Acid secretion

How do proteins stimulate gastric acid secretion during the gastric phase?

Partially digested proteins and amino acids → Stimulate G cells in the pylorus (antrum) → ↑ Gastrin → ↑ HCl secretion.

Additional note:

Pepsinogen is released by chief cells.

HCl converts pepsinogen → Pepsin, which digests proteins.

How does the intestinal phase regulate gastric acid secretion?

Protein digestion products enter the duodenum → Stimulate G cells → ↑ Gastrin → ↑ HCl secretion.

Fat and acid enter the small intestine → Stimulate release of secretin and CCK → ↓ Gastric acid secretion.

How does H. pylori survive in the stomach, and what diseases can it cause?

Bacterium that lives in the gastric mucus layer; often asymptomatic.

Produces urease, which converts urea → CO₂ + ammonia.

Ammonia neutralizes stomach acid, protecting the bacteria.

what percentage of the population has H. Pylori + what is the problem with this?

more than 50% - problem is sudden gastric cancer is possible + pts with H.pylori are asymptomatic

what complication can happen to most people with H.pylori ?

the infection remains confined to the antrum but leads

to increased acid secretion and

symptomatic inflammation that causes

ulceration of the stomach or duodenum

almost all duodenal peptic (acid-associated) ulcers and about half of gastric peptic ulcers have what shared root cause?

H.pylori

what are the remaining half of gastric peptic ulcers caused by?

remaining gastric ulcers are caused by medications (aspirin,

NSAIDs)

What stimulates CCK secretion?

Fat entering the small intestine.

What stimulates gallbladder contraction and bile flow?

Fat in the intestine stimulates CCK release from I cells → gallbladder contracts + sphincter of Oddi relaxes → bile enters duodenum.

What regulates gallbladder contraction and sphincter of Oddi relaxation?

Hormonal and neural inputs

Where is CCK secreted from?

I cells of the small intestine.

What are villi, and what is their function?

Projections of the intestinal mucosa into the lumen (~1 mm tall).

Increase absorptive capacity 5-fold.

Allow nutrients absorbed by enterocytes to enter circulation.

What are microvilli, and what is their function?

Tiny projections on the apical surface of enterocytes (3,000-5,000 per cell).

Increase absorptive surface area 200-fold.

Together form the brush border, which contains digestive enzymes.

What is lactase, and what happens when it is deficient?

Lactase is a brush border enzyme that digests lactose. (may lose over time)

↓ Lactase → Lactose intoleranc

What is the role of fluid and electrolyte secretion in the small intestine?

Flushes bacteria and toxins away from the intestinal epithelium → Mucosal defense.

What are secretagogues?

Substances that stimulate fluid and electrolyte secretion in the intestine.

What are the main types of secretagogues?

Neurotransmitters (submucosal plexus): VIP and acetylcholine.

Paracrines: Bradykinin, serotonin, histamine, and prostaglandins.

what are the neurotransmitter secretagogues?

these stimulate secretion : vasoactive intestinal peptide (VIP) and acetylcholine

What are Paracrine secretagogues?

bradykinin, serotonin, histamine, and prostaglandins

How do immune cells stimulate intestinal secretion?

Immune cell products → Activate submucosal neurons → Release acetylcholine or VIP → Stimulate enterocytes → ↑ Fluid and electrolyte secretion.

What are luminal secretagogues?

Bacterial toxins that stimulate intestinal fluid and electrolyte secretion.

Excessive intestinal secretion can lead to secretory diarrhea.

What are the main functions of the large intestine?

Absorbs water and electrolytes.

Secretes mucus.

Forms, propels, and stores feces.

Colon contains most of the gut bacteria.

how does the large intestine differ from the small intestine structurally?

No villi and few folds (except distal rectum).

Contains absorptive cells with microvilli and mucus-secreting goblet cells.

What cells are found in the colonic crypts?

Goblet cells

Endocrine cells

Absorptive cells

Epithelial stem cells → Replace cells that continuously shed.- so people poop even if they dont eat

Small intestine vs large intestine functions ?

Small intestine = nutrient absorption

large intestine = water absorption and feces formation.

How does digestion occur in the colon?

Colonic microbiota break down dietary fiber → Produce short-chain fatty acids (SCFAs) → Provide energy for colonic cells.

How do short-chain fatty acids protect the colon?

Promote survival of healthy colonic epithelial cells.

Induce apoptosis in cells progressing toward malignancy.

May help protect against colorectal cancer.

What is the colon's role in fluid and electrolyte absorption?

Can absorb up to 5 L of water/day.

Absorbs sodium even against its concentration gradient.

How does aldosterone affect the colon?

↑ Aldosterone → ↑ Sodium absorption in the colon → Helps maintain fluid and electrolyte balance, especially during volume depletion.

What are mucins, and where are they secreted?

large, highly glycosylated proteins secreted by goblet cells in the colonic epithelium.

What are the functions of mucins in the colon?

Protection: Form a hydrated mucus layer over the intestinal epithelium.

Lubrication: Prevent intestinal walls from sticking together.

Innate immunity: Form a barrier against bacteria and pathogens, along with antimicrobial peptides and immunoglobulins.

What is the gastrocolic reflex?

Colonic mass peristalsis after a meal, which moves stool through the colon.

How does diabetic autonomic neuropathy affect colonic motility?

Disrupts normal colonic motility → Can cause severe GI complaints.

What maintains stool continence?

Contraction of the puborectalis muscle and anal sphincters prevents stool from passing.

What happens during the defecation reflex?

Puborectalis relaxes → Straightens the anorectal angle, allowing stool to pass.

Rectal distension → Triggers reflex relaxation of the internal anal sphincter.

External anal sphincter → Relaxes voluntarily to allow defecation.

What causes GERD?

Decreased lower esophageal sphincter (LES) pressure or increased intra-abdominal pressure → Gastric contents reflux into the esophagus.

What conditions or factors contribute to GERD?

Hiatal hernia*

Decreased LES pressure

Increased intra-abdominal pressure

Delayed gastric emptying

When does GERD-related heartburn commonly occur?

30-60 minutes after eating or at night.

What complications can frequent gastric acid reflux cause?

Inflammation and ulceration of the esophageal mucosa → Eventually fibrosis and esophageal stricture (narrowing).

What factors decrease LES pressure and worsen GERD?

Caffeine

Fatty foods

Alcohol

Cigarette smoking

Certain medications

What are the epidemiologic characteristics of GERD?

BS

Prevalence in North America: 15.4%

No association between sex and GERD symptoms

Risk increases with advanced age

How common is regurgitation in infants?

Occurs in nearly 50% of newborns

Resolves spontaneously in 90% by age 1

What causes inflammation in GERD?

Gastric acid contacts the less acid-resistant squamous mucosa of the esophagus → Release of chemokines and cytokines → Inflammatory response.

What are the main mechanisms contributing to GERD?

Lower esophageal sphincter (LES) dysfunction

Esophageal hypersensitivity

Delayed gastric emptying

Increased gastroesophageal junction distensibility