GI Flashcards
What is the function of the GI tract?
- Food digestion
- Absorption of nutrients and water
What are the primary GI disorders?
- ) Damage 2⁰ to gastric acid secretion
- drugs- manage acid production
- )Abnormal food movement through the GI tract (gastric motility!!)
- excessive motility (diarrhea)
- reduced motility (constipation)
- management of emesis (N and V)
The gastrointestinal system is divided into what 2 parts?
- The GI tract
- Accessory digestive organs
What are the three phases of digestion?
Cephalic phase:
- anticipation of food (sight, smell) initiates release of stomach acid
- parietal cells secrete acid (for pH between 1-4)
- mucoid cells secrete mucus for stomach lining protection
Gastric phase:
- gastrin released when antrum stretched
- triggers release of more gastric acid
Intestinal phase:
- chyme enters duodenum
- triggers negative feedback for reducing gastric acid/ proteolytic enzyme action in stomach
- release of bicarbonate solution and pancreatic enzymes to aid in digestion
Control of digestion is divided into ______ control and _______ control
neuronal and hormonal
Neuronal control consists of what mainly?
- Enteric nervous system: myenteric plexus and submucosal plexus
- parasympathetic
- Sympathetic system
- decreases motility
- controls mucus secretion
- increases sphincter control
Hormonal control consists of what?
- Gastrin- stimulate gastric acid secretion
- Pepsinogen- converts to pepsin, digests proteins
- Secretin- stimulates pancrease to secrete HCO3 sol
- Cholecystokinin- stimulates gallbladder release of HCO3
- Others
What is essential for activating digestive protease activity and controlling intestinal bacteria?
Gastric acids (HCl)
Gastric acids can also do what?
Can cause severe ulceration of stomach lining with accompanying hemorrhage if produced excessively or if stomach lining is damaged.
Acid reducing agents work by stopping this process, block proton pump
2 acid-related GI conditions
- Peptic Ulcer
- GERD
What are peptic ulcers?
Ulceration of the mucosal lining of the esophagus, stomach, and/or duodenum
What is GERD?
Gastroesophageal reflux disease
-stomach contents leak backwards from the stomach into the esophagus (AKA: heartburn or acid indigestion)
Acid-suppressive drugs: Antacids MOA?
AE?
-neutralize gastric acidity
- AE: effervescent types (ie Alka-seltzer) have high sodium contents
- magnesium products- diarrhea
- aluminum and calcium- constipation
- DD interactions
- alter absorption of electrolytes from GI tract = e- inbalance
- avoid taking within 2 hrs of other oral medication
What is the primary use of Antacids?
- treat acid reflux
- increase stomach pH from 1.3 to 3.5 which produces symptomatic relief and some ulcer healing
What are some examples of antacids?
- calcium carbonate (tums)
- magnesium hydroxide (milk of magnesia)
Acid-suppressive drugs: Proton Pump Inhibitors MOA?
AE?
-irreversibly inhibits H+/K+ ATPase pump on parietal cell membrane which blocks final step in acid secretion into lumen of stomach
- generally well tolerated
- long term use associated with gastric polyps, altered calcium metabolism, some CV abnormalities
What is the primary purpose of Proton Pump Inhibitors?
-treat acid reflux and heal ulcers
Which has been shown to be more effective in treating acid reflux and healing ulcers: PPI or H2 Antagonist?
PPI
What are three mucosal protectors?
- Bismuth chelate
- Sucralfate
- Misoprostol
What can H. pylori infections cause?
What is used to treat it?
-chronic gastritis, PUD, GERD, gastric cancer
-Combination therapy: acid-controlling drug + antibiotic
Ex:
-colloidal bismuth, tetracycline, and metronidazole
-PPI plus 2 antibiotics
Treatment can eliminate bacteria within _____
1 week
What do we need to do with NSAID induced ulcers?
treat H. pylori infection plus add acid suppression therapy
discontinue NSAID if possible
What is involved in the regulation of vomiting?
- Chemoreceptor trigger zone (CTZ)
- floor of 4th ventricle in cerebrum
- responds to toxins/drugs in blood, CSF
- Vomiting center
What drugs are used to treat nausea and vomiting?
Antimetics
- Anticholinergics: used to prevent motion sickness relating vomiting
- Antihistamines: used to prevent motion sickness related vomiting
- Neuroleptic drugs: antipsychotic agents, some have anticholinergic actions
- Prokinetic drugs: produce central and peripheral antiemetic effects
- Serotonin blockers: prevent vomiting (emesis)
- Neurokinin-1 receptor blockers: newer class of drug to prevent emesis from chemotherapy
- Cannabinoids: block acute and delayed emesis, used for chemo-induced nausea/vomiting
Anticholinergics MOA?
Examples?
AE?
Anticholinergics:
- MOA- binds to ACh receptors on vestibular nuclei, blocks communication
- Ex- scopolamine
- AE- dizziness, drowsiness, dry mouth, blurred vision, dilate pupils, difficulty w/ urination
Antihistamines MOA?
Examples?
AE?
Antihistamines:
- MOA- inhibit vestibular input to the CTZ
- Ex- H2 blockers
- AE- dizziness and sedation
Neuroleptic drugs MOA?
Examples?
AE?
Neuroleptic drugs:
- MOA- block dopamine receptors in CTZ
- Ex- drugs for post-op nausea/vomiting, drugs for chemo induced vomiting
- AE- OH, tachycardia, blurred vision, dry eyes, urinary retension, long-term use can lead to extrapyramidal symptoms
- *tardive dyskinesia
Prokinetic drugs MOA?
AE?
Prokinetic drugs:
- MOA- blocks dopamine in CTZ
- AE- sedation, diarrhea, weakness, prolactin release, prolonged use can cause extrapyramidal signs
Serotonin blockers MOA?
AE?
Serotonin blockers:
- MOA- blocks seretonin receptors in GI tract, CTZ, and vomiting center
- AE- HA, dizziness, diarrhea, (no extrapyramidal signs)
What may be used in combination with serotonin blockers to control chemo-induced emesis?
Corticosteroids
Neurokinin-1 receptor blockers MOA?
AE?
Neurokinin-1 receptor blockers:
- MOA- blocks substance P from binding to NK-1 receptor, preventing both central and peripheral stimulation of vomiting centers
- AE- sedation, GI issues,…**Steven Johnsons syndrome
Cannabinoids MOA?
AE?
Cannabinoids:
- MOA- unclear
- AE- ataxia, light-headedness, blurred vision, dry mouth, weakness, tachy or bradycardia, CNS symptoms
Drug used to treat nausea and vomiting?
Antinausea
Phosphorated carbohydrate solution (Emetrol)- reduces nausea by working directly on walls of GI tract
Phosphorated carbohydrate solution MOA?
-MOA- relaxes GI tract smooth muscle
What is phosphorated carbohydrate solution used for?
Mild cases of intestinal flu or food-borne causes
What is the typical cause of diarrhea?
Water and electrolyte imbalance in intestinal tract
Common pathologies associated with diarrhea?
- IBS
- Crohn’s disease
- Ulcerative colitis
What are the 4 antidiarrheal agents?
- Absorbents
- Anticholinergics
- Intestinal flora modifiers
- Opiates
Absorbents MOA?
AE?
- binds to bacteria causing diarrhea and carry them out with feces
- aspirin product: use with caution in children recovering from flu/chickenpox
Decrease effectiveness of many drugs
Anticholinergics MOA?
AE?
- reduce peristalsis of GI tract
- Because of AE, rarely first choice for treatment
Intestinal flora modifiers MOA?
- bacterial products found from lactobacillus organisms
- normally resides in intestines to keep “bad” bacteria in check
- helps restore normal balance to suppress harmful organisms
Oppiates MOA?
AE?
- decrease GI motility and propulsion
- slowing transmit time in intestines= absorption of water and electrolytes
-sedation, dizziness, constipation, nausea, vomiting, respiratory depression
Constipation causes and treatments?
Causes:
- bowel impaction
- endocrine or neurological condition
- sedentary lifestyle
- poor diet
- medications
Treatments:
- surgery
- laxitives
What are the types of laxitives?
- Bulk forming
- Hyperosmotic
- Emollient
- Saline
- Stimulant
Bulk forming laxitives MOA?
-increase water absorption which softens and increases bulk of intestinal contents
Bulk-forming laxitives are generally ____.
Who shouldnt take these?
- safe
- individuals with abdominal pain, nausea, vomiting
What do you want to do with bulk forming laxitives?
Drink lots of water with these!
Hyperosmotic laxitives MOA?
AE?
- creates gradient that draws fluid into colon to increase stool fluid content and stimulate periostalsis
- abdominal bloating, rectal irritation, electrolyte imbalance
Emollient laxitives MOA?
AE?
- facilitate water and fat absorption into stool, lubricate fecal matter and intestinal wall
- skin rash, decreased vitamin absorption, electrolyte imbalance
What are emollient laxitives known as?
fecal softeners and lubricant laxitives
Saline laxitives MOA?
AE?
- simmilar to hyperosmotic- osmotic pressure pushes water/electrolytes into intestines
- salts may cause issues with individual with diminished cardiac or renal function
Stimulant laxitive MOA?
AE?
- stimulates peristalsis through enteric nervous system
- danger of long term use: dependence and damage to intestinal cells/loss of colon function
Therapeutic concerns with GI agents
- Patient positioning- should be lying flat (supine)
- avoid increased intra-abdominal pressure
- avoid exercise immediately after meals
- Dehydration
- Constipation
- Drug interactions
