upper gi Flashcards
Appetite controlled by
hypothalamus
Stimulated by hypoglycemia, empty stomach, decreased body temperature, brain input
Deglutition: swallowing
Includes mouth, pharynx, and esophagus
Absorption
occurs in the small intestine (villi)
Digestion is completed in the
small intestine.
Carbohydrates
Digestion starts in
mouth
Followed by digestion in the small intestine
Proteins
Digestion starts in
stomach, continues in small intestine
Lipids
Emulsified by
bile prior to chemical breakdown
Action of enzymes form monoglycerides and free fatty acids
Formation of chylomicrons
Fat-soluble vitamins
Vitamins A, D, E, K
Absorbed with fats
Water-soluble vitamins
Vitamins B and C—diffuse into blood
Electrolytes
Absorbed by active transport or diffusion
Drugs are primarily absorbed in the
intestine.
Various transport mechanisms
Some (e.g., aspirin) absorbed in the stomach
Gastric Secretion Phases
Cephalic (nervous)
–Secretion of hydrogen chloride (HCL), pepsinogen, mucus
Gastric (hormonal and nervous)
–Secretion of gastric hormone from antrum to stimulate gastric secretions
Intestinal (hormonal)
–Acidic chyme (pH <2): release of secretin, gastric inhibitory polypeptide, cholecystokinin
Chyme (pH >3): release of duodenal gastrin
Parasympathetic nervous system (PNS)
Primarily through vagus nerve (cranial nerve
[CN] X)
Increased motility
Increased secretions
Sympathetic nervous system (SNS)
Stimulated by factors such as fear, anger
Inhibits gastrointestinal activity
Causes vasoconstriction
Reduced secretions and regeneration of epithelial cells
which cranial nerves
Facial (CN VII) and glossopharyngeal (CN IX) nerves
Stomach empties within
2 to 6 hours after meal.
Gastrin
Secreted by mucosal cells (stomach) in response to distention of stomach or partially digested substances
Increases gastric motility, relaxes pyloric and ileocecal sphincters—promotes stomach emptying
Histamine
Increased secretion of hydrochloric acid
Secretin
Decreases gastric secretions
Cholecystokinin
Inhibits gastric emptying; stimulates contraction of gallbladder
Elimination
mainly happens in the large intestine
Haustral churning
what does pepsin breakdown
proteins
stomach forms
chyme
where does vit k synthesis happen?
in large intestine
if you throw up too much
alkalosis .
this aint important
and i might be wrong
Vomiting center located in the medulla
Coordinates activities involved in vomiting
Protects airway during vomiting
Presence of blood—hematemesis
- Coffee ground vomitus—brown granular material indicates action of HCl on hemoglobin
- Hemorrhage—red blood may be in vomitus
Yellow- or green-stained vomitus
Bile from the duodenum
Deeper brown color
May indicate content from lower intestine
Recurrent vomiting of undigested food
Problem with gastric emptying or infection
Diarrhea
May be accompanied by cramping pain
Prolonged may lead to: dehydration, electrolyte imbalance, acidosis, malnutrition
Large-volume diarrhea (secretory or osmotic)
Watery stool resulting from increased secretions into intestine from the plasma
Often related to infection
Limited reabsorption because of reversal of normal carriers for sodium and/or glucose
Small-volume diarrhea
Often caused by inflammatory bowel disease
Stool may contain blood, mucus, pus
May be accompanied by abdominal cramps and tenesmus
Steatorrhea—“fatty diarrhea”
Frequent bulky, greasy, loose stools
Foul odor
Characteristic of malabsorption syndromes
Celiac disease, cystic fibrosis
Fat usually the first dietary component affected
Presence interferes with digestion of other nutrients.
Abdomen often distended
Frank blood
Red blood—usually from lesions in rectum or anal canal
Occult blood
Small hidden amounts, detectable with stool test
May be caused by small bleeding ulcers
(happens in the small intestine or higher)
Melena
Dark-colored, tarry stool
May result from significant bleeding in upper digestive tract
(GI bleed)
types of gas
- Eructation - belching
- Borborygmus – rumbling or gurgling noise made by movement of fld/gass
- Abdominal distention and pain
- Flatus (post surgery people gots to do this)
Chronic constipation may cause
hemorrhoids, anal fissures, or diverticulitis.
normal BM can range from
3/day to q 3 days
Causes of Constipation
Weakness of smooth muscle - age or illness Inadequate dietary fiber Inadequate fluid intake Failure to respond to defecation reflex Immobility Neurological disorders Drugs (i.e., opiates) Some antacids, iron medications Obstructions caused by tumors or strictures
normal fiber intake
(25- 30 mq day)
Dehydration and hypovolemia are common complications
of digestive tract disorders.
Metabolic alkalosis
Results from loss of hydrochloric acid with vomiting
Metabolic acidosis
Severe vomiting causes a change to metabolic acidosis because of the loss of bicarbonate of duodenal secretions.
Diarrhea causes loss of bicarbonate.
PQRST
P = Provocation / Palliation Q = Quality / Quantity R = Region / Radiation S = Severity Scale T = Timing
Referred Pain
Results when visceral and somatic nerves converge at one spinal cord level
Source of visceral pain is perceived as the same as that of the somatic nerve.
REVIEW SLIDE 55
.
Causes of limited malnutrition—specific problem
Vitamin B12 deficiency
Iron deficiency
Radiological studies
Upper gastrointestinal series (barium swallow) Lower gastrointestinal series (barium enema) Abdominal ultrasonography (May show unusual masses) Computed tomography (CT) - (we get radiation from this_ so watch out) (its slices shit so you can find stuff like an acute bleed, stroke, i might be wrong about that ) Magnetic resonance imaging (MRI)
Endoscopy (Biopsy may be done during procedures)
Endoscopic ultrasonography
Capsule endoscopy
Sigmoidoscopy and colonoscopy
Liver function serum studies
Liver function, pancreatic function, cancer markers
Laboratory analysis of stool specimens
Check for infection, parasites and ova, bleeding, tumors, malabsorption
upper GI drugs
Antacids
To relieve pyrosis
Antiemetics
To relieve vomiting
Laxatives or enemas
Treatment of acute constipation
Antidiarrheals
Reduction of peristalsis
Relieve cramps
Sulfasalazine
Anti-inflammatory and antibacterial
Used for acute episodes of inflammatory bowel disease
Clarithromycin or azithromycin
Effective against Helicobacter pylori infection
Usually combined with a proton pump inhibitor
Sucralfate
Coating agent
Enhance gastric mucosal barrier against irritants such as nonsteroidal anti-inflammatory drugs (NSAIDs)
Anticholinergic drugs
Reduce PNS activity
Reduce secretions and motility
Histamine 2 antagonists
Useful for gastric reflux
Proton pump inhibitors
Reduce gastric secretion
Neurological deficit of dysphagia
Infection
Stroke
Brain damage
Achalasia (Failure of the lower esophageal sphincter to relax because of lack of innervation)
pancreatitis can sometimes show as
shoulder pain
appendix
usually starts with the whole stomach and then narrows down to one place
when you take x rays you gotta watch out for
preggos, watch out for thyroids. we got to cover the thyroid and protect reproductive.
always turn them to their lefts
when doing anything like enemas
Dysphagia
Causes:
-Neurological deficit (stroke, infection, Achalasia
Failure of the lower esophageal sphincter to relax because of lack of innervation)
-Muscular disorder
-Mechanical obstruction
(Congenital atresia (abnormal narrowing)- Developmental anomaly. Upper and lower esophageal segments are separated. AND Stenosis- Narrowing of the esophagus. AND Esophageal diverticula
Outpouchings of the esophageal wall )
Hiatal Hernia
Protrusion of the stomach through the esophageal hiaus of the diaprhragm into the throx.
Sliding hernia
More common type
Portions of the stomach and gastroesophageal junction slide up above the diaphragm
Rolling or paraesophageal hernia
Part of the fundus of the stomach moves up through an enlarged or weak hiatus in the diaphragm and may become trapped.
Hiatal Hernia: Assessment
Signs:
Pyrosis (Heartburn)
Frequent belching
Increased discomfort when laying down
Substernal pain that may radiate to shoulder and jaw
Feeling fullness after eating or a feeling of breathlessness or suffocation
Symptoms worse when lying down
Gastroesophageal Reflux Disease (GERD)
- Periodic reflux of gastric contents into distal esophagus causes erosion and inflammation.
- Often seen in conjunction with hiatal hernia
- Severity depends on competence of the lower esophageal sphincter.
- Delayed gastric emptying may be a factor.
GERD: Assessment
Consumption of: fatty foods, caffeinated beverages, chocolate, nicotine, alcohol, peppermint
Drug history: beta-blockers, calcium channel blockers, nitrates, anticolinergic drugs, estrogen & progesterone
Inflammation, discomfort up to 2 h after each meal
Regurgitation with a sensation of warm fluid traveling upward to the throat, leaving a bitter, sour taste in the mouth
Dysphagia
Flatulence and/or bloating after eating
Collaborative care
GERD
Lifestyle modifications
• Weight loss and smoking cessation
Nutritional therapy
• Reducing fatty foods, caffeinated beverages, chocolate, nicotine, alcohol, peppermint, intake of spicy and acidic foods.
• Eat 5 – 6 small meals during the day (decreases pressure
Drug therapy
• Antacids - neutralizes gastric acid
• Proton pump inhibitor (PPI) – most powerful!! Blocks final step in the H+ion secretion by the parietal cell
• Cispride and Metroclopramide – GI stimulants – improves gastric emptying
Surgical therapy
Teach patients to avoid factors that cause reflux:
Smoking cessation
Elevating HOB to 30 degrees (6” blocs under HOB)
Avoid lying down 2-3 hours after eating
Avoid late-night eating (3 h before sleep)
Avoid restrictive clothing, lifting heavy objects, straining, working bend over.
Gastritis
Inflammatory process of the mucosal lining of the stomach.
Acute:
gastritis
Alcohol or ingestion of aspirin or NSAIDs **
Infection by microorganisms
Ingestion of excessive amounts of tea, coffee, mustard, cloves, paprika or pepper
Ingestion of corrosive or toxic substances
Radiation or chemotherapy
Severe stress
Food poisoning (staph) and infections (candida, herpesvirus)
Usually self-limiting.
Complete regeneration of gastric mucosa
Supportive treatment with prolonged vomiting
May require treatment with antimicrobial drugs
May resolve in 48h (rapid cell proliferation and restoration of gastric mucosa)
Chronic:
gastritis
Type A – autoimmune
Type B – Helicobacter pylori
Long-term F/U gastric CA
Pernicious anemia (destruction of parietal cells in fundus and body leads to inadequate vitamin B12 absorption)
H2 Receptor antagonist – bocks gastric secretion and maintains pH of gastric contents above 4.0 thus decreasing inflammation
Antibiotics – treat H. pylori
Gastritis: Manifestations
Discomfort with facial grimaces and restlessness
Anorexia, nausea, vomiting may develop
Hematemesis caused by bleeding
Epigastric pain, cramps or general discomfort
With infection, diarrhea may develop.
Gastritis: Gastroenteritis
Inflammation of stomach and intestine
Microbes can be transmitted by fecally contaminated food, soil, and/or water
Escherichia coli Infection
Although E. coli is usually harmless as a resident in the human intestine, infective strains can cause significant problems.
Peptic Ulcer: Gastric & Duodenal Ulcers
Most caused by H. Pylori infection
Usually occur proximal duodenum
Both the acute and the chronic ulcers may penetrate the entire wall of the stomach.
.
Damage to mucosal barrier predisposes to development of ulcers and is associated with
- Inadequate blood supply
- Excessive glucocorticoid secretion or medication
- Ulcerogenic substances break down mucous layer.(like asprin, nsaids, etoh)
- Atrophy of gastric mucosa
- Increased acid pepsin secretions
Signs and symptoms and diagnostic tests:
peptic ulcer
Epigastric sharp, gnawing or burning localized pain,
Duodenal ulcer occurs 90m to 3h after eating, relieved with food or antacids
Gastric ulcer pain is precipitated by foo and not relieved by antacid
Diagnostic tests
Esophagogastroduodenoscopy
Barium x-ray
Peptic Ulcer: Treatment
Combination of
• antimicrobial – to eradicate H. Pylori
• proton pump inhibitor – optimizes ulcer healtin by binding to the proton pump of parietal cell and inhibiting secretion of H+ ions into gastric lumen
• H2 antagonist – reduces acid secretion to optimize ulcer healing
Reduction of exacerbating factors
Complications of peptic ulcer
Hemorrhage
• Caused by erosion of blood vessels
• Common complication
• May be the first sign of a peptic ulcer
Perforation
• Ulcer erodes completely through the wall.
• Chyme can enter the peritoneal cavity.
• Results in chemical peritonitis
Obstruction
• May result later because of the formation of scar tissue.
Age-Related Considerations: Peptic Ulcer Disease
Incidence in patients over 60 years of age is increasing.
(Related to increased use of NSAIDs)
In the older adult, pain may not be the first symptom associated with an ulcer.
Stress Ulcers
Associated with severe trauma or systemic problems
- -Burns, head injury
- -Hemorrhage or sepsis
Rapid onset
- -Multiple ulcers (usually gastric) may form within hours of precipitating event
- -First indicator—hemorrhage and severe pain
causes of dysphagia
- fibrosis
- compression( like a tumor)
- diverticulum (like a pouch that was formed and now blocks tube)
neurological defects ACHALASIA OR STENOSIS (which is the narrowing of the tube)
