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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
Q

Anticholinergics MOA?
Examples?
AE?

A

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
Q

Antihistamines MOA?
Examples?
AE?

A

Antihistamines:

  • MOA- inhibit vestibular input to the CTZ
  • Ex- H2 blockers
  • AE- dizziness and sedation
27
Q

Neuroleptic drugs MOA?
Examples?
AE?

A

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
Q

Prokinetic drugs MOA?

AE?

A

Prokinetic drugs:

  • MOA- blocks dopamine in CTZ
  • AE- sedation, diarrhea, weakness, prolactin release, prolonged use can cause extrapyramidal signs
29
Q

Serotonin blockers MOA?

AE?

A

Serotonin blockers:

  • MOA- blocks seretonin receptors in GI tract, CTZ, and vomiting center
  • AE- HA, dizziness, diarrhea, (no extrapyramidal signs)
30
Q

What may be used in combination with serotonin blockers to control chemo-induced emesis?

A

Corticosteroids

31
Q

Neurokinin-1 receptor blockers MOA?

AE?

A

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
Q

Cannabinoids MOA?

AE?

A

Cannabinoids:

  • MOA- unclear
  • AE- ataxia, light-headedness, blurred vision, dry mouth, weakness, tachy or bradycardia, CNS symptoms
33
Q

Drug used to treat nausea and vomiting?

Antinausea

A

Phosphorated carbohydrate solution (Emetrol)- reduces nausea by working directly on walls of GI tract

34
Q

Phosphorated carbohydrate solution MOA?

A

-MOA- relaxes GI tract smooth muscle

35
Q

What is phosphorated carbohydrate solution used for?

A

Mild cases of intestinal flu or food-borne causes

36
Q

What is the typical cause of diarrhea?

A

Water and electrolyte imbalance in intestinal tract

37
Q

Common pathologies associated with diarrhea?

A
  • IBS
  • Crohn’s disease
  • Ulcerative colitis
38
Q

What are the 4 antidiarrheal agents?

A
  • Absorbents
  • Anticholinergics
  • Intestinal flora modifiers
  • Opiates
39
Q

Absorbents MOA?

AE?

A
  • 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
Q

Anticholinergics MOA?

AE?

A
  • reduce peristalsis of GI tract

- Because of AE, rarely first choice for treatment

41
Q

Intestinal flora modifiers MOA?

A
  • 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
Q

Oppiates MOA?

AE?

A
  • decrease GI motility and propulsion
    • slowing transmit time in intestines= absorption of water and electrolytes

-sedation, dizziness, constipation, nausea, vomiting, respiratory depression

43
Q

Constipation causes and treatments?

A

Causes:

  • bowel impaction
  • endocrine or neurological condition
  • sedentary lifestyle
  • poor diet
  • medications

Treatments:

  • surgery
  • laxitives
44
Q

What are the types of laxitives?

A
  • Bulk forming
  • Hyperosmotic
  • Emollient
  • Saline
  • Stimulant
45
Q

Bulk forming laxitives MOA?

A

-increase water absorption which softens and increases bulk of intestinal contents

46
Q

Bulk-forming laxitives are generally ____.

Who shouldnt take these?

A
  • safe

- individuals with abdominal pain, nausea, vomiting

47
Q

What do you want to do with bulk forming laxitives?

A

Drink lots of water with these!

48
Q

Hyperosmotic laxitives MOA?

AE?

A
  • creates gradient that draws fluid into colon to increase stool fluid content and stimulate periostalsis
  • abdominal bloating, rectal irritation, electrolyte imbalance
49
Q

Emollient laxitives MOA?

AE?

A
  • facilitate water and fat absorption into stool, lubricate fecal matter and intestinal wall
  • skin rash, decreased vitamin absorption, electrolyte imbalance
50
Q

What are emollient laxitives known as?

A

fecal softeners and lubricant laxitives

51
Q

Saline laxitives MOA?

AE?

A
  • simmilar to hyperosmotic- osmotic pressure pushes water/electrolytes into intestines
  • salts may cause issues with individual with diminished cardiac or renal function
52
Q

Stimulant laxitive MOA?

AE?

A
  • stimulates peristalsis through enteric nervous system

- danger of long term use: dependence and damage to intestinal cells/loss of colon function

53
Q

Therapeutic concerns with GI agents

A
  • 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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