10.2 - Pathophysiological Conditions of the Stomach Flashcards
What are the causes of Gastritis?
gastritis - inflammation of the stomach lining
Causes:
1) Infection - H.Pylori
2) Medications
NSAIDs - can erode gastric mucosa
3) Alcohol and Tobacco Use
- Irritate and inflame gastric lining
4) Autoimmune Conditions
Body attacks its gastric cells = impaired acid production
What is the Pathology of Gastritis?
1) H Pylori Infxn
- H pylori triggers immune cells to release pro-inflammatory cytokines to remove bacteria, but H pylori can evade immune clearance
- This persistent immune response leads to ongoing inflammation of stomach lining and damage gastric epithelium
2) Mucosal Injury
- due to NSAID’s and alcohol disrupt mucosal barrier = susceptible to acid damage
3) Autoimmune Mechanisms
- Self-attack of parietal cells ↓ acid production & vitamin B12 absorption
How do NSAID’s disrupt mucosal barrier?
- NSAIDs COX (cyclooxygenase) inhibitors by blocking the COX-1 and COX-2 enzymes
COX-1
- Enzyme in stomach produces prostaglandins
- Promotes production of mucus & bicarbonate (basic)
- protect stomach lining from stomach acid
- Maintain blood flow to the stomach lining
COX-2
- Produces prostaglandins that mediate inflammation, pain, and fever
NSAIDs inhibit COX-1 andCOX-=↓ production of protective prostaglandins in stomach = ↓mucus & bicarbonate secretion = more acidic stomach AND ↓ blood flow to the stomach = lining vulnerable to damage
What are the Structural Changes of Gastritis?
1) Erosions
- Loss of the gastric mucosa due to inflammation
2) Atrophy
- Chronic cases = thinning of gastric mucosa & loss of glandular structures
3) Intestinal Metaplasia
- metaplastic changes increases cancer risk
What is the clinical Significance of Gastritis?
S&S
- Epigastric pain
- nausea
- vomiting & hematemesis (uncommon)
Complications
- ↑ risk of peptic ulcer disease
- gastric carcinoma
- vitamin B12 deficiency
Management
- Antibiotics for H. pylori,
- proton pump inhibitors
- lifestyle changes
Causes of Peptic Ulcer Disease
PUD - development of open sores in lining of stomach or duodenum
1) H pylori - most common;
- leads to chronic inflammation and ulcer formation
2) NSAID - disrupts gastric mucosal barrier increasing acid vulnerability
3) Zollinger -Ellison Syndrome - increases gastric secretions and results in high acids stomach levels
4) Smoking, alcohol use, stress - can exacerbate ulcer disease
Pathogenesis of Peptic Ulcer Disease
1) Mucosal damage due to acid & pepsin
- H. pylori infection or NSAID weaken mucosal defenses = stomach acid erodes lining & causes inflammation = deeper tissue damage & ulcer formation
2) Acid-Pepsin Interaction
Pepsinogen = pepsin = breaks down stomach lining & contributes to tissue injury & ulceration
- Pepsin digests proteins but also digests the stomach and dudeonal tissues if protective mucosal barrier is compromised
- In nomral conditions, stomach and duodenum are protected by thick layer containing bicarbonate that neutralizes the stomach acid and buffer effects of pepsin
□ This barrier is weakened due to NSAID’s or H pylori etc
Structural Changes of Peptic Ulcer Disease
1) Ulcer Formation
- Mucosa eroded = exposure of deep layers = bleeding & perforation
2) Fibrosis & Scar Tissue
Fibrosis = strictures = ↓ gastric or duodenal flexibility
Clinical Significance of Peptic Ulcer Disease
S&S
- Burning epigastric pain (worse on empty stomach or at night)
- nausea or vomiting
Complications
- Bleeding
- perforation (leading to peritonitis)
- gastric outlet obstruction
- ↑ risk of gastric cancer in H. pylori-related ulcers
Management
- Antibiotics for H. pylori
- acid suppression with proton pump inhibitors
- lifestyle modifications
Causes of Gastric Cancer
- Adenocarcinoma; arises from stomach lining
1) Infection
- Chronic H. pylori
- Epstein-Barr Virus (EBV) infection
2) Diet
- Smoked, salted, and pickled foods
3) Genetic Factors
- Family history
- genetic mutations (e.g., CDH1 gene, TP53 tumor suppressor gene)
4) Environmental Factors
- Smoking, obesity, and exposure to environmental toxins
Pathogenesis of Gastric Cancer
1) Chronic Gastritis and Atrophy
- Persistent inflammation = mucosal atrophy
2) Intestinal Metaplasia and Dysplasia
- Persistent inflammation & tissue damage = gastric epithelial cells transform into intestinal-like phenotype
3) Carcinoma Development
- Accumulated mutations and dysplasia = cells proliferate abnormally = invading surrounding tissue & eventually metastasizing
Structural Changes of Gastric Cancer
1) Mucosal Changes
- H. pylori-associated inflammation = gastric mucosa atrophy & intestinal metaplasia
2) Ulceration and Mass Formation
3) Lymphatic and Blood Vessel Invasion
- Advanced cancer infiltrates lymphatic and blood vessels = metastasis
Clinical Significance of Gastric Cancer
Symptoms
- Early-stage gastric cancer asymptomatic or vague symptoms like indigestion
- Advanced symptoms include weight loss, anemia, abdominal pain, and vomiting
Complications
- Bleeding
- obstruction
- METS to liver & lymph nodes
Management
- Surgical resection
- chemotherapy
- targeted therapies for specific genetic mutations
Causes of Gastroenteritis
Gastroenteritis: Inflammation of stomach and intestines usually caused by infection
1) viruses
Norovirus and rotavirus
2) Bacteria
E.coli, Salmonella,
3) Parasites
Pathogenesis of Gastroenteritis
1) Virus-Induced Gastroenteritis
- Invade & damage intestinal mucosal cells = disrupting fluid & electrolyte absorption
2) Bacterial Gastroenteritis
- Produce toxins (e.g., Vibrio cholerae’s cholera toxin) = stimulate excessive secretion of water & electrolytes
Invade & destroy mucosal cells = inflammation & ulceration
3) Parasitic Infections
- Attach to or invade mucosa = inflammation and damage to villi = impaired nutrient absorption
Structural Changes of Gastroenteritis
1) Mucosal damage
- Mucosal cell death & villous atrophy
2) Edema and Inflammation
- Mucosal edema & inflammatory = fluid loss & ↑ mucus production
3) Ulceration and Erosions
- Severe bacterial infections
Clinical Significance of Gastroenteritis
S&S
- Diarrhea
- vomiting
- If client has excessive vomiting, will experiencing metabolic alkalosis: they vomited all the acid out of the body (body is too alkaline)
- abdominal pain
- dehydration and electrolyte imbalance (metabolic alkalosis)
Complications
- Dehydration
- electrolyte imbalances (metabolic alkalosis), and malnutrition
- Children & older adults are ↑ risk
Management
- Rehydration/ electrolyte replacement
- ABX (bacterial cases)
Causes of Gastric Paresis
Gastric paresis - disorder where stomach motility fails and stomach fails to empty food peorly into intestines
- Impaired stomach motility = delayed gastric emptying
1) Diabetes Mellitus
- Long-standing hyperglycemia = damages the vagus nerve = neuropathy = ↓ gastric motility
2) Surgical Injury
- Surgical damage to vagus nerve
3) Idiopathic (unknown) Causes
4) Medications
- Opioids; can slow gastric emptying
Pathogenesis of Gastric Paresis
1) Vagal Nerve Damage
- Damage to the vagus nerve = impaired signals to stomach muscles = ↓ gastric contractions
2) Smooth Muscle Dysfunction
Impaired muscle response = ↓ stomach propulsion
3) Impaired Gastric Pacemaker
- Dysfuction of interstitial cells of Cajal = impaired motility
Structural Changes of Gastric Paresis
1) Delayed Gastric Emptying
- Stomach remains distended, food & liquid accumulate
2) Reduced Gastric Tone and Motility
- Musculature less responsive to normal stimuli = stasis
3) Potential for Bezoar Formation
- Food in stomach clumps together = bezoars
- Bezoars - massive indigestible material that increases risk of other complications
Clinical Significance of Gastric Paresis
S&S
- Nausea
- vomiting
- early satiety
- bloating
- weight loss; due to inadequate digestion and nutrient absorption
Complications
- Recurrent vomiting & malnutrition
- DM with gastroparesis = unstable blood glucose levels (bec bolus of food in stomach affects glucose metabolism)
Management
- Diet modifications, prokinetic agents
- surgical intervention (i.e., gastric stimulator implant to aid in motility)
Causes of Hiatal Hernia
Hiatal hernia - when part of stomach pushes upward through diaphragm and enters thoracic cavity
1) Increased intra-abdominal pressure
- Obesity, pregnancy, and chronic coughing
2) Age-related changes
- Weakening of the diaphragm with age
3) Congenital factors
- Born with an abnormally large hiatus
Pathogenesis of Hiatal Hernia
1) Sliding Hiatal Hernia
- Gastroesophageal junction & part of stomach slide into thorax
2) Paraesophageal Hernia
- Portion of stomach herniates beside the esophagus, gastroesophageal junction remains in normal anatomical location
Structural Changes of of Hiatal Hernia
1) Herniated Stomach
- Stomach or gastroesophageal junction moves into chest cavity
2) Reduced Lower Esophageal Sphincter (LES) Pressure
- Impaired closure of LES = reflux
Clinical Significance of Hiatal Hernia
Symptoms
- Asymptomatic
- heartburn
- regurgitation
- dysphagia
- chest pain
Complications
- GERD
- esophagitis or strangulation of herniated stomach
Management
- Lifestyle modifications
- proton pump inhibitors
- surgical repair
