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Pharmacology > Elimination > Flashcards

Elimination Flashcards

1
Q

What is Elimination?

A

The excretion of waste products through stool.

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2
Q

What are the three parts of the GI tract?

A
  1. the upper tract: mouth, esophagus and stomach
  2. the lower tract: the duodenum, jejunum and ileum
  3. the lower tract: the cecum, colon and rectum
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3
Q

What is the role of the upper esophageal sphincter?

A

The pharyngoesophageal sphincter creates a zone of high pressure that serves to prevent reflux of gastric contents into the esophagus.

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4
Q

What is the role of the parietal cells?

A

They secrete HCL

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5
Q

What is the role of the chief cells?

A

They secrete pepsinogen

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6
Q

What is the role of the goblet cells?

A

They secrete mucus

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7
Q

What is the role of enterochromaffin cells?

A

They secrete histamine and serotonin

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8
Q

What is the role of the G cells?

A

They release gastrin

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9
Q

What is the sequelae of HCL secretion?

A

G cells-Gastrin-Enterochromaffin cells-Histamine-Parietal Cells-HCL secretion

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10
Q

What is the target pH of the stomach?

A

pH= 1.5-3.5!

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11
Q

Define endogenous protection.

A

The stomach itself must protect itself from the highly acidic environment. Endogenous Protection refers to the natural defence against stomach acid

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12
Q

Where are the parietal cells located?

A

The gastric pits of the stomach!

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13
Q

What is GERD?

A

Gastroesophageal Reflux Disease (GERD). ccurs when stomach acid flows back into the esophagus (Acid Reflux)
The backflow causes irritation and damage to the esophageal mucosal lining creates a “burning” sensation and heartburn

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14
Q

Signs and Symptoms of GERD.

A
  • Regurgitation
  • Sore Throat
  • Cough
  • Chest Pain
  • Dysphagia
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15
Q

Describe the physiology of GERD.

A

The lower esophageal sphincter is closed at rest, which prevents gastric content from refluxing into the esophagus. The most common trigger of acid reflux is spontaneous relaxation of the LES, usually triggered by gastric distention after meals.

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16
Q

What are the three-drug classes used to treat GERD?

A
  1. Antacids
  2. Proton Pump Inhibitors
  3. Histamine-2- Receptor antagonsits
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17
Q

What is an antacid?

A

They are used to neutralize the acid in the esophagus however, do not heal the damaged tissue.

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18
Q

What is a Proton Pump Inhibitor?

A

PPI’s inhibit the H+, K+ ATPase proton pump. Not only do they control gastric secretions they promote mucosal healing.

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19
Q

What are histamine-2-receptor antagonists?

A

used to treat GERD by inhibiting histamine adhesion at the H2 receptors on parietal cells. Inhibiting the activation of the parietal cells and decreasing HCL secretion

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20
Q

Define Fundoplication.

A

an operation where the superior portion of the fundus is wrapped around in order to narrow the esophageal sphincter

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21
Q

What is Peptic Ulcer Disease?

A

a condition in which painful sores or ulcers develop in the lining of the stomach or the first part of the small intestine (the duodenum). Caused by mucosal erosion

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22
Q

What are the traits of a Gastric Ulcer?

A
  • Pain is increased after meal
  • Anorexia
  • Hematemesis
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23
Q

What are the traits of a duodenal ulcer?

A
  • Pian relieved with food
  • Normal Appetite
  • Melana stool
24
Q

What is H. Pylori?

A

A gram-negative bacterium that adheres to the stomach lining and releases ammonia, which degrades the mucosal lining, causing erosion and ultimately peptic ulcers.

25
Q

How is H.Pylori Diagnosed?

A

Through the presence in stool samples

26
Q

How do NSAID’s influence the development of peptic ulcers?

A

NSAID interferes with the stomach’s capability of protecting itself from gastric acids, causing the stomach lining to be exposed. NSAID’s inhibit the release of prostaglandins which are essential for mucus production/secretion

27
Q

How do you treat H-pylori?

A
  • 3 antibiotics for 2 weeks
    1. Amoxicilin
    2. Clarythromycin
    3. Metronidazole (flagyl)
  • Proton Pump Inhibitor
  • Bismuth Therapy
28
Q

What are the two biggest clinical concerns in regards to the GI tract?

A
  1. Diarrhea (too fast)

2. Constipation (too slow)

29
Q

What are the indicators of Non-Inflammatory acute diarrhea?

A
  • watery
  • no melena stool
  • dehydration
30
Q

What are the indicators of Inflammatory acute diarrhea?

A
  • Caused by a pathogenic invasion
  • Fever and melena stool
  • Lower quadrant cramps
  • Result in dehydration
31
Q

What is C. Difficile?

A

A Gram-negative bacteria that cause inflammatory diarrhea. It spread easily, multiplies quickly, and does not die from anti-bacterial gel. It also has a high antibiotic resistance.

32
Q

How is C.Difficile Treated?

A

Flagyl and Vancomycin

33
Q

How does Flagyl work?

A

Inhibits protein synthesis by interacting with DNA and causing a loss of helical DNA structure and strand breakage.

34
Q

How does Vancomycin work?

A

Vancomycin, long considered a “drug of last resort,” kills by preventing bacteria from building cell walls.

35
Q

How to treat Acute Diarrhea?

A
  • Rehydrate! (Isotonic IV solution)
  • Encourage fluid intake
  • Antidiarrheals
36
Q

What is IBS?

A

A disorder that affects the large intestine. Irritable bowel syndrome, a functional disorder. Causing cramping, abdominal pain, bloating and gas.

37
Q

What is IBD?

A

Inflammatory Bowel Disease: causes inflammation, ulcer and other damage to the bowel. (IBD) is a term for two conditions (Crohn’s disease and ulcerative colitis) that are characterized by chronic inflammation of the gastrointestinal

38
Q

What factors influence/ cause constipation?

A
  • Increase in dietary fibre
  • Decrease in water intake
  • Decreased peristalsis
39
Q

What questions do you ask the patient to assess constipation?

A
  • How often do you have a bowel movement?
  • What is the consistency of the stool?
  • Do you have any sharp abdominal pain?
  • LATERSNAPS
40
Q

What is Hirchussprung Disease?

A

Is caused when the parasympathetic ganglion cells in the wall of the colon deteriorate. Without these nerves, the colon lacks the ability to relax and move bowel contents. This birth defect causes chronic constipation.,

41
Q

What are the 5 classes of laxatives used to treat constipation?

A
  • Osmotic
  • Stool softeners
  • Bulk-forming
  • Stimulants/Irritants
  • Lubricating
42
Q

How do osmotic laxatives work?

A

They pull water into the stool, softening the stool and allowing the contents to move. ex. Milk of magnesia

43
Q

How do Stool softeners work?

A

They pull water AND fat into the stool to soften the contents

44
Q

How do bulk-forming laxatives work?

A

They pull water into the stool and add bulk to the contents. The fibre increases the bulk of the stool and the water follows the fibre. A patient on bulk-forming laxatives must be hydrated!

45
Q

How do stimulants work?

A

They stimulate peristalsis movements and irritate the GI tract to increase mobility and excrete the contents. This is not the first choice as it causes pain and can cause perforation (a hole through the intestine)

46
Q

What causes bloating?

A

Gas!

47
Q

How do you treat bloating?

A

Bloating is treated with enzymes to increase carbohydrate digestion!

48
Q

What triggers nausea and vomiting?

A

Nausea and vomiting is triggered by the introduction of a toxin within the GI system or from motion sickness

49
Q

Pathophysiology of nausea and vomiting?

A

When the GI tract is stimulated it signals to the medulla through the vagal afferent nerve and activates the emetic centre (vomiting centre) and the chemoreceptor trigger zone, which then stimulates the abdominal muscles to start cramping in an attempt to regurgitate the contents in the stomach.

50
Q

How do you treat nausea?

A

Antiemetics!

51
Q

How does Ginger work?

A

Ginger is an NHP and increases intestinal peristalsis to promote the movement of the contents out of the system!

52
Q

Function of Antihistamines for Nausea.

A

(H1 Antagonism): used to treat motion-induced sickness by reducing vestibular excitation

53
Q

The function of Ginger gravol for Nausea.

A

Increases intestinal peristalsis. Within the gastrointestinal tract, ginger gravol will help by increasing gastric tone and motility due to its anticholinergic effects and increasing gastric emptying. Therefore, getting rid of the toxins that created nausea.

54
Q

The function of Antimuscarinic Anticholinergics for Nausea.

A

Reduce vestibular excitation. Anticholinergics refer to agents that block cholinergic receptors, (acetylcholine receptors). Muscarinic antagonists, block muscarinic cholinergic receptors, bronchodilation, increasing heart rate, and inhibiting secretions.

55
Q

The Function of Serotonin Antagonists for Nausea.

A

Inhibits serotonin. Antagonists block serotonin both peripherally on vagal nerve terminals in the gastrointestinal (GI) system and centrally in the chemoreceptor trigger zone.

56
Q

The Function D2 Receptor Antagonists for Nausea.

A

They inhibit dopaminergic neurotransmission in the brain by blocking the D2 dopamine receptors. They can also block noradrenergic, cholinergic, and histaminergic activity. drugs that bind to and inhibit or block the activation of dopamine d2 receptors.

57
Q

The Function of CB1 and 2 Agonists for Nausea,

A

Cannabinoid receptor agonists. These cause an inhibitory effect and inhibit sympathetic nervous system activity. Therefore, reducing feelings of nausea and slowing down peristaltic movements.

Pharmacology (27 decks)

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