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Pharmacology Exam 2 > GI > Flashcards

GI Flashcards

1
Q

What is the function of the GI tract?

A
  • Food digestion

- Absorption of nutrients and water

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2
Q

What are the primary GI disorders?

A
  1. ) Damage 2⁰ to gastric acid secretion
    • drugs- manage acid production
  2. )Abnormal food movement through the GI tract (gastric motility!!)
    • excessive motility (diarrhea)
    • reduced motility (constipation)
    • management of emesis (N and V)
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3
Q

The gastrointestinal system is divided into what 2 parts?

A
  • The GI tract

- Accessory digestive organs

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4
Q

What are the three phases of digestion?

A

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
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5
Q

Control of digestion is divided into ______ control and _______ control

A

neuronal and hormonal

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6
Q

Neuronal control consists of what mainly?

A
  • Enteric nervous system: myenteric plexus and submucosal plexus
    • parasympathetic
  • Sympathetic system
    • decreases motility
    • controls mucus secretion
    • increases sphincter control
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7
Q

Hormonal control consists of what?

A
  • 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
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8
Q

What is essential for activating digestive protease activity and controlling intestinal bacteria?

A

Gastric acids (HCl)

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9
Q

Gastric acids can also do what?

A

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

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10
Q

2 acid-related GI conditions

A
  • Peptic Ulcer

- GERD

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11
Q

What are peptic ulcers?

A

Ulceration of the mucosal lining of the esophagus, stomach, and/or duodenum

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12
Q

What is GERD?

A

Gastroesophageal reflux disease

-stomach contents leak backwards from the stomach into the esophagus (AKA: heartburn or acid indigestion)

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13
Q

Acid-suppressive drugs: Antacids MOA?

AE?

A

-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
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14
Q

What is the primary use of Antacids?

A
  • treat acid reflux

- increase stomach pH from 1.3 to 3.5 which produces symptomatic relief and some ulcer healing

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15
Q

What are some examples of antacids?

A
  • calcium carbonate (tums)

- magnesium hydroxide (milk of magnesia)

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16
Q

Acid-suppressive drugs: Proton Pump Inhibitors MOA?

AE?

A

-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
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17
Q

What is the primary purpose of Proton Pump Inhibitors?

A

-treat acid reflux and heal ulcers

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18
Q

Which has been shown to be more effective in treating acid reflux and healing ulcers: PPI or H2 Antagonist?

A

PPI

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19
Q

What are three mucosal protectors?

A
  • Bismuth chelate
  • Sucralfate
  • Misoprostol
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20
Q

What can H. pylori infections cause?

What is used to treat it?

A

-chronic gastritis, PUD, GERD, gastric cancer

-Combination therapy: acid-controlling drug + antibiotic
Ex:
-colloidal bismuth, tetracycline, and metronidazole
-PPI plus 2 antibiotics

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21
Q

Treatment can eliminate bacteria within _____

A

1 week

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22
Q

What do we need to do with NSAID induced ulcers?

A

treat H. pylori infection plus add acid suppression therapy

discontinue NSAID if possible

23
Q

What is involved in the regulation of vomiting?

A
  • Chemoreceptor trigger zone (CTZ)
    • floor of 4th ventricle in cerebrum
    • responds to toxins/drugs in blood, CSF
  • Vomiting center
24
Q

What drugs are used to treat nausea and vomiting?

Antimetics

A
  • 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
25
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
26
Antihistamines MOA? Examples? AE?
Antihistamines: - MOA- inhibit vestibular input to the CTZ - Ex- H2 blockers - AE- dizziness and sedation
27
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
28
Prokinetic drugs MOA? | AE?
Prokinetic drugs: - MOA- blocks dopamine in CTZ - AE- sedation, diarrhea, weakness, prolactin release, prolonged use can cause extrapyramidal signs
29
Serotonin blockers MOA? | AE?
Serotonin blockers: - MOA- blocks seretonin receptors in GI tract, CTZ, and vomiting center - AE- HA, dizziness, diarrhea, (no extrapyramidal signs)
30
What may be used in combination with serotonin blockers to control chemo-induced emesis?
Corticosteroids
31
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
32
Cannabinoids MOA? | AE?
Cannabinoids: - MOA- unclear - AE- ataxia, light-headedness, blurred vision, dry mouth, weakness, tachy or bradycardia, CNS symptoms
33
Drug used to treat nausea and vomiting? | Antinausea
Phosphorated carbohydrate solution (Emetrol)- reduces nausea by working directly on walls of GI tract
34
Phosphorated carbohydrate solution MOA?
-MOA- relaxes GI tract smooth muscle
35
What is phosphorated carbohydrate solution used for?
Mild cases of intestinal flu or food-borne causes
36
What is the typical cause of diarrhea?
Water and electrolyte imbalance in intestinal tract
37
Common pathologies associated with diarrhea?
- IBS - Crohn's disease - Ulcerative colitis
38
What are the 4 antidiarrheal agents?
- Absorbents - Anticholinergics - Intestinal flora modifiers - Opiates
39
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
40
Anticholinergics MOA? | AE?
- reduce peristalsis of GI tract | - Because of AE, rarely first choice for treatment
41
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
42
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
43
Constipation causes and treatments?
Causes: - bowel impaction - endocrine or neurological condition - sedentary lifestyle - poor diet - medications Treatments: - surgery - laxitives
44
What are the types of laxitives?
- Bulk forming - Hyperosmotic - Emollient - Saline - Stimulant
45
Bulk forming laxitives MOA?
-increase water absorption which softens and increases bulk of intestinal contents
46
Bulk-forming laxitives are generally ____. | Who shouldnt take these?
- safe | - individuals with abdominal pain, nausea, vomiting
47
What do you want to do with bulk forming laxitives?
Drink lots of water with these!
48
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
49
Emollient laxitives MOA? | AE?
- facilitate water and fat absorption into stool, lubricate fecal matter and intestinal wall - skin rash, decreased vitamin absorption, electrolyte imbalance
50
What are emollient laxitives known as?
fecal softeners and lubricant laxitives
51
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
52
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
53
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

Pharmacology Exam 2 (7 decks)

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