disorders of the GI system

Signs and Symptoms Common to Gastrointestinal Disorders

1. anorexia

2. nausea

3. vomiting (emesis)

4. GI bleeding

Anorexia:

:Decreased appetite, often triggered by illness ,pain, or emotional stress

Anorexia nervosa

Intentional food restriction due to distorted body image, leading to severe weight loss and electrolyte imbalance.

nausea

Unpleasant sensation often described as “queasy” or “sick to the stomach”

•   Initiated by the vomiting center in the medulla

•   Triggered by GI distention, motion, pain, smells, or

  psychological cues

Vomiting (Emesis)

Reflexive ,forceful expulsion of stomach contents through the mouth

•  Coordinated by the vomiting center in the medulla

vomitting is influenced by?

• signals from the GI tract, vestibular system, higher brain centers, and the chemoreceptor trigger zone (CTZ)

  ◼ CTZ detects toxins in blood and CSF—important in drug- and toxin-induced vomiting

vomitting involves?

•   Involves activation of salivary glands, respiratory muscles, and abdominal contraction

•   Neurotransmitters involved: dopamine and serotonin (targets for anti-nausea drugs)

Hematemesis

•   Vomiting of blood

•   May appear bright red (fresh) or dark with a coffee ground appearance (partially digested)

Hematochezia

 Passage of bright red blood in stool

 Usually indicates bleeding from the lower GI tract (e.g., colon, rectum)

 Blood coating the stool often suggests hemorrhoids

melena

 Black, tarry stool caused by digested blood

 Typically indicates bleeding above the ileocecal valve (e.g., stomach or duodenum)

 May lead to elevated BUN due to nitrogen absorption from digested blood

occult bleeding

0.  Hidden blood in the stool, not visible to the eye

    Detected by chemical tests (e.g., fecal occult blood test)
    Common causes: gastritis, peptic ulcers, or small intestine lesions

swallowing mechanism

requires precise coordination of the tongue and pharynx

Disruption can occur from neurological damage (e.g., stroke) or

structural issues (e.g., esophageal strictures)

swallowing controlled by

Controlled by cranial nerves V (trigeminal), IX

(glossopharyngeal), X (vagus), and XII (hypoglossal)

dysphagia

 Difficulty swallowing
 May involve problems initiating a swallow or food getting "stuck" in the throat or chest

odynophagia

 Pain with swallowing

gerd

Backward flow of stomach contents into the esophagus, causing heartburn

and irritation

•   Stomach lining is protected from acid; the esophagus

  is not, leading to mucosal damage

•   Often due to a weak or incompetent lower

  esophageal sphincter (LES)

gerd symptoms

•   Epigastric or retrosternal pain; may radiate to the throat, shoulder, or back

•   Heartburn severity does not predict extent of damage

•   May also cause wheezing, chronic cough, or

  hoarseness (from acid irritating the larynx)

Chronic reflux may lead to (GERD)

◼ Strictures (narrowing from scar tissue)

◼ Barrett’s esophagus: squamous cells replaced with columnar cells → ↑ risk of esophageal cancer

GERD treatment

• ◼  Eat smaller, more frequent meals to reduce stomach pressure pushing against LES

• ◼  Stay upright during and after meals – gravity helps keep contents down

• ◼  Elevate the head of the bed to reduce nighttime reflux

• ◼  Lose weight if overweight – excess abdominal fat raises pressure on the LES

• ◼  Use acid-reducing meds as needed – antacids, H2 blockers, or proton pump inhibitors (PPIs)

GERD avoid:

• ◼  Avoid trigger foods (spicy, acidic, tomato-based, etc.) that worsen reflux

• ◼  Avoid alcohol and smoking – both relax the lower esophageal sphincter

  (LES) and increase acid

• ◼  Avoid lying flat for 2–3 hours after eating

• ◼  Limit bending or stooping after meals – this increases abdominal pressure

• ◼  Avoid medications that irritate the GI tract or reduce mucosal protection (e.g., NSAIDs)

major causes of gastric irritation & ulcer formation

1. Helicobacter pylori infection

2. NSAIDs (e.g., aspirin, ibuprofen)

3. Alcohol, smoking, and caffeine

4. stress

helicobacter pylori infection causing ulcer formations

 This bacterium can survive harsh acidic stomach conditions by

producing an enzyme called urease
 Disrupts the mucosal barrier
 Triggers inflammation and epithelial injury

how do NSAIDS cause ulcers

 Inhibit prostaglandin synthesis, reducing mucosal protection

 This is enhanced with concurrent corticosteroid use

how does alcohol, smoking and caffeine cause ulcers

 Increase acid production and reduce mucosal defense

how does stress cause ulcers

 Increases acid secretion
 Decreases mucosal blood flow and regeneration

Detection of H. pylori Infection

1. Urea Breath Test

2. Stool Antigen Test

3. Endoscopic Biopsy (with Urease Testing)

4. serologic Blood Test

Urea Breath Test

 Patient swallows urea labeled with a carbon isotope

 If H. pylori is present, it breaks down the urea → labeled CO2 is exhaled

 Non-invasive and accurate

Stool Antigen Test

 Detects H. pylori proteins in the stool
 Commonly used to confirm eradication after treatment

endoscopic Biopsy (with Urease Testing)

 Sample taken during upper endoscopy

 Tests for urease enzyme activity or histology

 Most direct and reliable, but invasive

Serologic Blood Test

 Detects antibodies to H. pylori
 Cannot distinguish active vs past infection

examples of physiological stress

Large surface-area burns

Trauma
Sepsis

Acute respiratory distress syndrome

Severe liver failure
Major surgical procedures

Cushing Ulcer

examples of psychological stress

From increased levels of cortisol

acute gastritis

 Sudden, short-term inflammation of the gastric lining

 Often self-limiting once irritant is removed

acute gastritis common causes

alcohol, NSAIDs (e.g., aspirin), stress, spicy food

acute gastritis treated with

◼ Antacids, H2 blockers, proton pump inhibitors (PPIs)

◼ Sucralfate to coat and protect the stomach lining

chronic gastritis

 Long-term inflammation with no obvious erosions
 Leads to atrophy of glandular epithelium and reduced acid/enzymes

type sof chronic gastritis

1. H. pylori Gastritis

2. Autoimmune Gastritis

• Autoimmune Gastritis

• antibodies attack parietal cells, reducing intrinsic factor → can lead to vitamin B12 deficiency

◼ May require B12 supplementation

• H. pylori Gastritis

• most common; requires antibiotics + PPI

peptic ulcer

sore or erosion in the lining of the stomach or duodenum

peptic ulcer caused by?

breakdown of mucosal defenses due to acid and pepsin

Erosion may extend into deeper layers, and in severe cases, all the way to the peritoneum

most common types of peptic ulcers

 Gastric ulcers (in the stomach)

 Duodenal ulcers (in the first part of the small intestine)

gastric ulcers

Ulcers form in the mucosa of the stomach and may

extend into the submucosa

risk factors of gastric ulcers

 H. pylori infection

 NSAID use (aspirin, ibuprofen)
 Smoking, alcohol, stress
 History of gastritis or previous gastric ulcers

clinical features of gastric ulcers

• Pain WORSENS with eating (and typically 1–2 hours after a

  meal)
  ◼ Gnawing or sharp pain in the mid or left epigastric region

•  Nausea and vomiting

  ◼ Hematemesis:

  “Coffee ground” emesis from digested blood

  Bright red blood if not digested

duodenal ulcers

Ulceration occurs in the mucosa of the duodenum (usually the proximal portion)

clinical features of duodenal ulcers

• Pain IMPROVES with food (temporarily neutralizes acid)

• Burning or gnawing pain in the mid-epigastric area

• Pain occurs 2–4 hours after eating or during the night (when stomach is empty)

• May present with melena (black, tarry stools from digested blood)

complications of peptic ulcers

1. pain

2. hemorrhage

3. gastric outlet obstruction

4. perforation

pain from peptic ulcers

Ongoing epigastric discomfort is the most common

symptom

hemorrhage from peptic ulcers

Ulcer erosion into blood vessels can cause significant bleeding

 Occult bleeding: Chronic, slow blood loss may lead to iron-deficiency anemia

gastric outlet obstruction from peptic ulcers

 Caused by inflammation, muscle spasm, or scar tissue near the pylorus

 Interferes with the passage of gastric contents into the duodenu

peforation from peptic ulcers

 Full-thickness erosion through the stomach or duodenal wall

 Leads to peritonitis, a surgical emergency

zolligner Ellison syndrome

Caused by a gastrin-secreting tumor (gastrinoma), usually in pancreas or duodenum

•   Excess gastrin → excessive gastric acid → recurrent, treatment- resistant ulcers

•   More than two-thirds of tumors are malignant

Zollinger Ellison syndrome clinical features

 Multiple ulcers
 Abdominal pain, nausea, vomiting
 Chronic diarrhea, steatorrhea (fat malabsorption)
 Weight loss
 Elevated fasting serum gastrin
 GI bleeding (hematemesis or melena)
 GERD symptoms
 metabolic alkalosis (due to excessive HCl production)

 Hypokalemia (potassium shift due to alkalosis)

ZE syndrome causes?

metabolic alkalosis

Vitamin B12 Deficiency

◼ Results from either an inadequate intake of vitamin B12 or a lack of absorption of ingested vitamin B12 from the intestinal tract

pernicious anemia results from a

deficiency of intrinsic factor (IF), which is necessary for intestinal absorption of vitamin B12

Vitamin B12 Deficiency assessment

 Severe pallor/Fatigue due to anemia

 Weight loss due to anorexia
 Smooth, beefy red tongue – glossitis
 Paresthesias – numbness/tingling in hands and feet from nerve damage

 Gait and balance problems – due to impaired proprioception
 Slight jaundice – from increased breakdown of immature RBCs

Vitamin B12 Deficiency Treatment

 Oral Vit. B12 (if inadequate intake) or IM Vit. B12 (if lacking IF)

Irritable Bowel Syndrome (IBS)

• Chronic, recurrent abdominal pain with no structural or cellular abnormalities

• Diagnosis based on symptoms; no specific lab or imaging test

• Thought to result from dysfunction in the brain–gut axis, which controls GI motility and sensation

common symptoms of IBS

 Alternating constipation and diarrhea
 Bloating, gas, and abdominal discomfort

IBS more common in?

• women; symptoms may worsen during menstruation

   Hormonal fluctuations (e.g., estrogen and progesterone) likely contribute to symptom flare-ups

Normal WBC

IBD

structural damage and inflammation and tissue damage of the GI tract,

IBD has?

Elevated WBC count: Reflects immune activation during disease flare-ups; helps monitor inflammation and potential complications

Crohn’s disease

•   Chronic autoimmune inflammation that can affect any part of the GI

  tract (mouth to anus)

•   Involves all layers of the bowel wall

•   Lesions are patchy ("skip lesions")

ulcerative colitis

 Chronic autoimmune inflammation limited to the colon and rectum

 Affects only the mucosal layer
 Inflammation is continuous (no skip lesions)

IBD vs IBS

IBD involves structural damage and inflammation and tissue damage of the GI tract, while IBS is a functional disorder without visible inflammation or tissue damage

Crohn’s disease most common in

terminal ileum and cecum

crohns disease involves

Involves T cells and macrophages attacking the intestinal wall.
◼ Trigger may include altered gut microbiome or barrier dysfunction

 “Skip lesions,” strictures, ulcers, perforation, fistulas, and abscesses

 Marked by remissions and flare-ups

crohns clinical features

 Crampy abdominal pain

 Diarrhea (usually non-bloody)
 Weight loss and fatigue
 Anemia (iron and B12 malabsorption)

 Dehydration
 Strictures may cause bowel obstruction

fistulas

Abnormal tunnels from the bowel to other organs or skin that can Cause

leakage, infections, and poor healing

abscesses

Pockets of pus from deep infection

• Can lead to pain, fever, and seriouscomplications like sepsis

ulcerative colitis

• Chronic autoimmune inflammation that begins in the rectum and extends upward through the colon.

   Limited to the mucosa and submucosa (no skip lesions)
   Leads to bleeding ulcers and impaired nutrient absorption

   Periods of flare-ups and remission

ulcerative colitis may form:

• pseudopolyps (regenerative mucosal projections)

polyp

• A true growth of new tissue that sticks out from the lining of the colon. Some types can turn into cancer over time.

pseudopolyp

• Not a true growth, just leftover bits of normal tissue between ulcers. Common in ulcerative colitis. These do not become cancerous

• Colonic carcinoma:

• Ulcerative colitis increases colon cancer risk over time due to repeated inflammation and healing, not because pseudopolyps turn malignant.

complication of ulcerative colitis

• Risk of perforation with deep ulcers

• ◼  Complication: toxic megacolon (paralyzed, dilated colon that may rupture)

ulcerative colitis manifestations

◼Severe diarrhea with blood and mucus

◼Abdominal tenderness and cramping

◼Dehydration and electrolyte imbalances

◼ Anemia

◼Weight loss
◼ Anorexia
◼ Malaise
◼Vitamin K deficiency (due to loss of gut flora which predominately live in colon)

Diverticulosis

 Formation of small outpouchings (diverticula) in the intestinal wall

 Usually asymptomatic; most common in the sigmoid colon

 Linked to aging and low-fiber diets

Diverticulitis

 Inflammation of one or more diverticula

 Caused by trapped stool or bacterial overgrowth

 Risk of perforation, which can lead to peritonitis and sepsis

diverticulitis manifestations

• Left lower quadrant abdominal pain (most common; location

  of sigmoid colon)

• Guarding

• Fever and elevated WBC count/CRP (signs of inflammation)

• Nausea and vomiting (often due to ileus or inflammation)

• Change in bowel habits (diarrhea or constipation)

• Blood in stool (from mucosal irritation or erosion)

• Pain worsens with straining, coughing, or lifting (increased intra-abdominal pressure)

• Risk of perforation (can lead to peritonitis and sepsis)

hemorrhoids

 Swollen veins in the anal canal due to increased venous pressure

 Triggers: straining (e.g., constipation, childbirth), prolonged sitting, low-fiber diet, portal hypertension

internal hemorrhoids

In rectum; usually painless; may cause bright red bleeding or mucus

external hemorrhoids

• External: Around anus; often painful and itchy; visibly swollen

They occur in areas where there are lots of sensory nerves

prolapsed hemorrhoids

Internal hemorrhoids that protrude outside the anus

key symptoms of hemorrhoids

• Bright red rectal bleeding

• Pain (especially if external or thrombosed)

• Itching, swelling, or mucus discharge

appendicitis

Inflammation of the appendix; risk of rupture leading to peritonitis and sepsis

appedicitis key features

•   Early (Visceral) Pain: Colicky, crampy, around the

  umbilicus

•   Later (Parietal) Pain: Sharp, steady pain in the right lower quadrant (McBurney’s point)

appendicitis assessment findings

• Rebound tenderness

• Guarding – muscle tension protecting inflamed area

• Anorexia, nausea, vomiting

• Low-grade fever, elevated WBC count

• Possible constipation or diarrhea

• Patient often lies still with knees drawn up to reduce pain

diarrhea

Normal: ≤150 g stool/day; diarrhea = ↑ stool volume or frequency

4 main causes of diarrhea

•   Increased secretion of water & electrolytes into the bowel

•   Increased osmotic load draws water into lumen (e.g., lactase deficiency)

•   Inflammation → protein & fluid exudate secreted from mucosa

•   Increased motility → reduced absorption time

manifestations of diarrhea

 Dehydration

 Electrolyte imbalances
 Malabsorption & weight loss

 Anal irritation

secretory diarrhea

Increased Fluid Secretion into intestinal lumen

• Large-volume watery diarrhea that doesn’t improve with fasting

1. cholera toxin

2. c difficult

3. villous adenoma

cholera toxin

from contaminated water; causes intestines to secrete chloride and water → rapid dehydration

c difficile

often after antibiotics kill normal gut bacteria; C. diff overgrows and releases toxins → damages colon lining → watery diarrhea, fever, cramping

villous adenoma

benign colon polyp that leaks mucus and electrolytes → chronic diarrhea

osmotic diarrhea

unabsorbed substances pull water into bowel by osmosis

diarrhea improves with fasting (less solute in bowel = less water pulled in)

1. lactose intolerance

2. sorbitol (sugar free gum and candy)

3. ocean water ingestion

4. celiac disease

lactose intolerance

undigested lactose ferments → gas, bloating, water pulled in → diarrhea

Sorbitol (sugar-free gum/candy)

poorly absorbed → stays in lumen and pulls water in by osmosis