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PATHO/PHARM II > Mod 3: Lecture 1 > Flashcards

Mod 3: Lecture 1 Flashcards

Exam 1

1
Q

Divisions of the GI system

A

Upper

Lower

Hepatobilliary system

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2
Q

Divisions of the GI system: Upper

A

Esophagus
Stomach
Small intestine

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3
Q

Divisions of the GI system: Lower

A

Large intestine (colon)
Appendix
Rectum

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4
Q

Divisions of the GI system: Hepatobilliary system

A

Liver, gallbladder, pancreas

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5
Q

Neural controls: Sympathetic nervous system- what does it decrease?

A

Decreases secretion and peristalsis

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6
Q

Neural controls: Parasympathetic nervous system- what nerve

A

Vagus nerve

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7
Q

Neural controls: Parasympathetic nervous system- does what?

A

Increases secretion and peristalsis

Tasting food

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8
Q

Neural controls: Sympathetic nervous system- what does it stimulate?

A

Stimulates vasoconstriction in the mucosa

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9
Q

What stomach enzyme digests proteins?

A

Pepsin

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10
Q

What does HCI do in the stomach?

A

HCl acid activates enzymes, breaks up food, kills germs

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11
Q

What protects the stomach walls?

A

Mucus protects stomach wall

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12
Q

What is an issue with the stomach?

A

limited absorption

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13
Q

Lower esophageal (cardiac) sphincter is where:

A

between esophagus and stomach

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14
Q

Pyloric sphincter is where:

A

between the stomach and duodenum

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15
Q

What protects gut wall of small intestine?

A

Mucus

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16
Q

What does small intestine do?

A

Absorbs nutrients and most water

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17
Q

What in small intestine digests proteins, what digests sugars? What digests nucleotides?

A

Peptidase digests protein
Sucrases digest sugar
Nucleotidases and phosphatases digest nucleotides

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18
Q

What does large intestine do?

A

Reabsorbs some water and ions
Forms and stores feces

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19
Q

What does rectum do?

A

Stores feces prior to elimination through anus

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20
Q

What organ completes digestion?

A

small intestine

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21
Q

Chyme

A

acid fluid passes partially digested food from stomach to small intestine

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22
Q

What are the digestive juices stomach makes:

A

Hydrochloric acid ~
Pepsin ~
Gastric lipase ~
Intrinsic factor ~
Mucus ~

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23
Q

How does HCI work?

A

is secreted by parietal cells,

protein digestion, kills bacteria

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24
Q

What does gastric lipase do?

A

Gastric lipase ~ fat digestion

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25
Q

What does intrinsic factor do?

A

Intrinsic factor ~ B12 absorption in small intestine

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26
Q

What is mucus stimulated by?

A

Mucus ~ Protects stomach lining,

stimulated by prostaglandins,

mucosal barrier, gastric mucosal blood flow

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27
Q

Stomach absorption of nutrient? What is absorbed in the stomach?

A

No nutrients, only prepares for absorption.

ETOH

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28
Q

Pyloric sphincter- what does it prevent?

A

Prevents reflux of bile from the small intestines

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29
Q

Pyloric sphincter

A

a muscular valve at the bottom of the stomach that controls the flow of food from the stomach into the small intestine

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30
Q

What is the initial part of the small intestine?

A

Duodenum

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31
Q

Emesis- what kind of action?

A

Involuntary or voluntary

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32
Q

How is emesis protective?

A

Drug OD
Infection

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33
Q

What is emesis associated with? What are examples?

A

Association with severe pain

ex;
Migraines
Renal calculi

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34
Q

What does emesis involve coordination with?

A

Coordination via medulla oblongata

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35
Q

Coordination via medulla oblongata for emesis include what two groups?

A
  1. Vomiting center (VC) activation
  2. Chemoreceptor Trigger Zone (CTZ)
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36
Q

What is needed for Vomiting center (VC) activation?

A

Direct acting stimuli

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37
Q

What are examples of direct acting stimuli in VC activation?

A

Fear ~ cerebral cortex
Smell/sight or pain ~ sensory organs
Motion sickness ~ vestibular apparatus of inner ear (cranial nerve VIII)

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38
Q

Fear is involved with what part of the brain?

A

Fear ~ cerebral cortex

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39
Q

Smell/sight or pain is involved with what part of the brain?

A

Smell/sight or pain ~ sensory organs

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40
Q

Motion sickness is involved with what part of the brain?

A

Motion sickness ~ vestibular apparatus of inner ear (cranial nerve VIII)

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41
Q

The Chemoreceptor Trigger Zone (CTZ) requires what kind of stimuli?

A

Indirect stimuli

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42
Q

Indirect stimuli for the CTZ include what?

A

Gut activation

Drugs, toxins, chemicals in the blood

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43
Q

Vomitus; What is it and does it aid with?

A

Contents vomited

Aids w/ ID of underlying cause

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44
Q

Hematemesis:

A

vomitus with blood

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45
Q

What kind of appearance does vomit with blood have? Why?

A

Brown, granular appearance ~ coffee grounds

It is Partially digested protein

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46
Q

Why does hematemesis occur?

A

Blood irritation to GI mucosa –> attempts to expel

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47
Q

Diagnosis is capable of causing upper GI bleed include

A

Gastric ulcers
Esophageal varices
GIB gastro intestinal bleeding

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48
Q

Bile containing vomitus is what color?

A

Yellow- or green-colored

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49
Q

Bile containing vomitus
Why does it occur?

A

Can occur from GI tract obstruction

Liver biliary

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50
Q

Fecal containing vomitus (throwing up poop); how does it appear? Why?

A

Deep brown color of

May indicate content from lower intestine, possibly fecal

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51
Q

Fecal containing vomitus (throwing up poop) diagnosis include:

A

Intestinal obstruction
Impacted feces
cancer

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52
Q

Undigested food in vomitus occur because:

A

Impaired gastric emptying
Pyloric stenosis

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53
Q

Projectile Emesis

A

Vomitus exits with force

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54
Q

What are qualities of projectile emesis?

A

Often sudden

Subsequent excessive vomitus with each attack

Are not preceded by nausea

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55
Q

Associated conditions of projectile vomitting? what is the main one?

A

Intestinal obstructions
Delayed gastric emptying

↑ ICP/Head injury

Poisoning
Overeating
Neurologic lesions – tumors, aneurysms- involving brainstem
Pyloric stenosis

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56
Q

Complications of Emesis include:

A

Exhaustion

Fluid imbalances

Electrolyte imbalances

Acid–Base imbalances -?

Aspiration

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57
Q

What kind of acid base imbalance from vomitting?

A

metabolic alkalosis

acidosis for diarrhea

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58
Q

Procedures for management of Emesis may include?

A

PMH
PE
Blood chem

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59
Q

What are treatment goals for management of emesis?

A

Cessation of vomiting

Maintaining hydration (PO/IVF)

Restoring acid–base balance

Correcting electrolyte alterations

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60
Q

For cessation of vomiting, what can be given?

A

Antiemetics

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61
Q

Antiemetics include

A

5HT antagonists
Metoclopramide
Antihistamines: Dimenhydrinate, Meclizine, Diphenhydramine
Muscarinic antagonist: scopolamine

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62
Q

Best management of motion sickness

A

Most effective to treat prophylactically

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63
Q

Scopolamine is what kind of drug?

A

Muscarinic antagonist

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64
Q

How does Scopolamine patch work?

A

TD patch behind the ear
Apply 4h prior to travel

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65
Q

What are examples of Antihistamines for motion sickness?

A

Dimenhydrinate & meclizine

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66
Q

Which is most effective for managing motion sickness?

A

Scopolamine

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67
Q

Receptors & Agents Involved in Emesis

What classes of drugs are involved in emesis control?

A
  1. Serotonin antagonists
  2. Anticholinergics
  3. Antihistamines
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68
Q

5HT3 receptor Antagonists (serotonin receptor antagonists)- What is the prototype?

A

Ondansetron (Zofran)

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69
Q

What class in Ondansetron (Zofran)?

A

Class: Serotonin antagonists

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70
Q

What is the mode of action of Ondansetron (Zofran)?

A

Blocks type 5HT-3 serotonin receptors in the CTZ & on afferent vagal nerves upper GIT

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71
Q

What is Ondansetron (Zofran) used for?

A

CINV
Radiation
Anesthesia

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72
Q

How is Ondansetron (Zofran) administered?

A

PO, IM or IV, ODT

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73
Q

What is Ondansetron (Zofran) augmented with?

A

Augmentation with GCs

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74
Q

How should Ondansetron (Zofran) for a procedure (chemo)?

A

Give before to prevent:

CINV 30min prior
Anesthesia 1h prior
Radiation TID
Postop N/V

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75
Q

COmmon adverse effects of Ondansetron (Zofran)?

A

HA, diarrhea, dizziness

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76
Q

What is a serious adverse effect of Ondansetron (Zofran)?

A

QT prolongation

↑ risk of torsades de pointes
Avoid in long QT syndrome

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77
Q

When should Ondansetron (Zofran) be avoided?

A

Avoid in long QT syndrome

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78
Q

What does Ondansetron (Zofran) not cause?

A

⍉ DA blockade = ⍉ EPS

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79
Q

Precautions to take for Ondansetron (Zofran)?

A

Electrolyte imbalances
HF
Brady dysrhythmias

QT prolonging drugs

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80
Q

Metoclopramide (Reglan) is what class of drug?

A

Prokinetic agent/Dopamine antagonist

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81
Q

Since Metoclopramide (Reglan) is a Prokinetic agent/Dopamine antagonist, what does that mean?

A

Increase GI tone & motility

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82
Q

What is the mode of action of Metoclopramide (Reglan) ?

A

Blockade of Dopamine & serotonin receptors in CTZ

Increases Ach actions = increase in upper GI motility

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83
Q

Metoclopramide (Reglan) causes Blockade of Dopamine & serotonin receptors in CTZ, what can this be used for?

A

CINV & post-op N/V

chemotherapy-induced nausea and vomiting

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84
Q

Since Metoclopramide (Reglan) increases acetylcholine actions and increases upper GI motilitywhat does that mean?

A

Stimulates motility of UGI tract & accelerates gastric emptying (rest & digest)

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85
Q

Metoclopramide (Reglan) Stimulates motility of UGI tract & accelerates gastric emptying (rest & digest); What does this mean it can be used for?

A

Diabetic gastroparesis
Suppression of gastroesophageal reflux

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86
Q

How is Metoclopramide (Reglan) administered?

A

PO

IV

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87
Q

When should Metoclopramide (Reglan) be administered for Diabetic gastroparesis ? How?

A

PO

Diabetic gastroparesis (10mg PO 30 min before meals & HS x 2-8 wks)

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88
Q

When should Metoclopramide (Reglan) be administered for gastroesophageal reflux? How?

A

PO

Suppression of gastroesophageal reflux (10-15mg PO 30 min before meals & HS for max 12 wks)

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89
Q

What is Metoclopramide (Reglan) given IV for?When?

A

CINV & post-op N/V ~ 30min prior

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90
Q

Adverse effects of Metoclopramide (Reglan)

A

Sedation & diarrhea- Common in High Dose therapy

Irreversibletardive dyskinesia

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91
Q

Since Metoclopramide (Reglan) causes tardive dyskinesia, what does this?

A

Keep TX brief!!!

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92
Q

What is Metoclopramide (Reglan) contraindicated in?

A

GI obstruction, perforation, or hemorrhage
as per ↑ GI motility

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93
Q

Key Nursing Responsibilities with Metoclopramide Administration:

A

Assess for Parkinsonian sx – diff speaking, swallowing, loss of balance, pill rolling, rigidity, tremors, dystonia and tardive dyskinesia – uncontrolled rhythmic movements of mouth, face, exts, lip smacking, puffing cheeks

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94
Q

What is the mode of action of scopolamine?

A

Suppressing nerve communication in neuronal pathway that connects the vestibular apparatus of inner ear to the vomiting center

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95
Q

What is released during vestibular system activation?

A

Acetylcholine

Vestibular apparatus –> XX inner ear XX –> VC

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96
Q

Scopolamine is used for what?

A

Most effective drug for preventing motion sickness

End Of Life

Scopolamine > antihistamines

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97
Q

How is Scopolamine administered?

A

Oral, Sq, transdermal
TD patch applied behind ear
Q72h

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98
Q

Common Adverse effects of Scopolamine?

A

Dry mouth, blurred vision, drowsiness

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99
Q

What are more severe but less common effects of scopolamine?

A

Urinary retention, constipation, disorientation

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100
Q

Antihistamine drugs include?

A

Dimenhydrinate (Dramamine)

Meclizine (Antivert)

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101
Q

Why are antihistamines classified as anticholingerics?

A

Classified as anticholinergic because block receptors for acetylcholine (muscarinic cholinergic)

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102
Q

Why are antihistamines mode of action?

A

Blockade of histamine (H1) & muscarinic receptors in the neuro pathway connecting inner ear to VC

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103
Q

What can antihistamines be used for?

A

Use: motion sickness

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104
Q

What are adverse effects of antihistamines?

A

H1 blockade

Muscarinic blockade

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105
Q

Adverse effects of antihistamines: H1 blockade means it leads to what symptoms?

A

Sedation

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106
Q

Adverse effects of antihistamines: muscarinic blockade means it leads to what symptoms??

A

Dry mouth, confusion, hallucinations

Blurry vision, urinary retention, constipation

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107
Q

Gastritis

A

Inflammatory disorder of the gastric mucosa lining

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108
Q

What does gastritic do to stomach lining?

A

Gastric lining red, edematous

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109
Q

What occurs when the stomach lining is damaged?

A

Ulceration and bleeding when the mucosal barrier is damaged, or circulation compromised

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110
Q

What are common causes of gastritis?

A

Drugs: *NSAIDs, Glucocorticoids

*H. pylori, physiologic stress-related mucosal changes

Alcohol, metabolic disorders (eg renal failure – uremia)

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111
Q

Symptoms of acute gastritis include?

A

Sx: vague abd pain, epigastric tenderness, bleeding

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112
Q

Who does Chronic gastritis tend to occur in?

A

Tends to occur in older adults

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113
Q

What does Chronic gastritis cause?

A

Causes gastric mucosal atrophy, epithelial changes

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114
Q

What are two types of chronic gastritis?

A

2 types: immune (T-cell toleranace, auto Abs) vs

non-immune (same causes as acute)

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115
Q

What is immune cause of chronic gastritis?

A

T-cell toleranace, auto Abs)

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116
Q

What is nonimmune cause of chronic gastritis?

A

non-immune (same causes as acute)

117
Q

What does chronic gastritis put you at an increased risk for?

A

Increased risk of duodenal ulcers, gastric cancer

118
Q

What is effects with chronic gastritis?

A

Absorption of nutrients and enzymes are affected

119
Q

How to treat chronic gastritis without medicine?

A

Eat small meals, soft, bland diet, avoid etoh & ASA

120
Q

What is treatment of chronic gastritis?

A

Tx: GI meds, abx for h.pylori, Vit B12

121
Q

Helicobacter pylori (H. Pylori) what kind of bacteria?

A

Gram neg bacteria adapts to acidic stomach by secreting toxins

122
Q

How does Helicobacter pylori (H. Pylori) survive in the stomach?

A

Gram neg bacteria adapts to acidic stomach by secreting toxins

123
Q

What does Helicobacter pylori (H. Pylori) do?

A

Invades the gastric mucosa lining, causing inflammation.

124
Q

What is important about the shape of H.pylori?

A

Spiral shape allows them to penetrate mucosal barrier, where they are protected by mucus, interfering in the immune response so they are not destroyed.

125
Q

What causes stomach irritation in H.Pylori? What else does it cause?

A

The combination of stomach acid and H. pylori cause irritation, resulting in sores and ulcerations.

126
Q

How long is H.pylori in the gut?

A

Can remain in gut for decades

127
Q

What are signs and symptoms of Helicobacter pylori (H. Pylori)?

A

S/sx: Excessive burping, bloating, n/v, anorexia, unexplained weight loss, foul breath

128
Q

How is H.Pylori assessed?

A

Tested through stomach lining endoscopic biopsy, breath, serologic, stool tests

129
Q

What does H.Pylori treatment consist of in general?

A

Combo of antibiotics prescribed (at least 2) to reduce risk of resistance (10-14 days)

130
Q

What antibiotics are used to treat H.pylori in combination? - name 4

A

Proton Pump Inhibitor (PPI) or HR2A blocker

Mucosal protectants

Amoxicillin (Pcn)

Clarithromycin (macrolide)

131
Q

What antibiotics are used to treat H.pylori in combination? - name 3

A

Bismuth compounds (bismuth subsalicylate - main ingredient in Pepto-Bismol)

Tetracycline

Metronidazole

132
Q

What does amoxicillin do to treat H.pylori?

A

Kills H. pylori by disrupting cell wall, highly sensitive

133
Q

Where does amoxicillin work highest?

A

Works highest at a neutral pH

134
Q

How are amoxicillin effects enhanced?

A

Effects enhanced by reducing gastric acidity with an antisecretory agent

135
Q

What is the most common side effect of amoxicillin?

A

Most common side effect is diarrhea

136
Q

What does Clarithromycin (macrolide) do for H.pylori treatment?

A

Suppresses growth of H. pylori by inhibiting protein synthesis

137
Q

What is the most common side effect of Clarithromycin (macrolide)?

A

Most common side effects: Nausea, Diarrhea, Distortion of taste

138
Q

What does Bismuth compounds (bismuth subsalicylate - main ingredient in Pepto-Bismol) do for H.pylori treatment?

A

Disrupt the cell wall of H. pylori

139
Q

What does Bismuth compounds (bismuth subsalicylate - main ingredient in Pepto-Bismol) may do to H.pylori?

A

May inhibit urease activity and may prevent H. pylori from adhering to the gastric surface

140
Q

What can Bismuth compounds (bismuth subsalicylate - main ingredient in Pepto-Bismol) cause as a harmless effect? **highlighted

A

Can impart a harmless black coloration to the tongue and stool (melena)

141
Q

What should be included in patient teaching of Bismuth compounds (bismuth subsalicylate - main ingredient in Pepto-Bismol) use? **highlighted

A

Long-term therapy: Possible risk of neurologic injury

142
Q

What does Tetracycline do to H.pylori?

A

Inhibitor of bacterial protein synthesis

143
Q

What can happen if tetracycline is used in pregnant/young children?

A

Use in pregnant patients/young children can stain developing teeth

144
Q

What is wrong with Metronidazole use for H.pylori?

A

Over 40% of strains are now resistant 

145
Q

Most common side effects of Metronidazole use for H.pylori?

A

Most common side effects are nausea and headache

146
Q

What happens if Metronidazole is used with alcohol

A

Disulfiram reaction if used with etoh

147
Q

Peptic Ulcer Disease is what?

A

Open sores on stomach’s protective mucosal lining or upper duodenum

148
Q

How can severe erosion in PUD be complicated?

A

Severe erosion can be complicated by hemorrhage and perforation

149
Q

How can PUD be?

A

Can be single, multiple, acute, chronic, superficial, deep

150
Q

What are causes of Peptic Ulcer Disease (PUD)?

A

Imbalance between protective mucosal < erosive factors

Most common cause - Infection with H. pylori

Second most common cause - NSAIDs

151
Q

What is the most common cause of PUD?
highlighted slide

A

Most common cause - Infection with H. pylori

152
Q

What are risk factors to peptic ulcer disease?

A

NSAIDs, H. pylori, stress, etoh, steroids, age, smoking

153
Q

What are signs and symptoms of Peptic Ulcer Disease (PUD)

A

epigastric/abd pain, cramps, heartburn, indigestion, CP, N/V, fatigue, unexplained wgt loss, hematemesis & melena (duodenal ulcers)

154
Q

What are three types of three types of Peptic Ulcers? What is the most common?

A

Duodenal ulcers (most common)

Gastric ulcers (stomach ulcers)

Stress Ulcers

155
Q

Types of Peptic Ulcers: What are Duodenal ulcers (most common) characterized by?

A

Characterized by intermittent pain in the epigastric area

156
Q

Types of Peptic Ulcers: When does pain associated with Duodenal ulcers occur?

A

Pain begins 2-3 hours after eating, when stomach empty

157
Q

Types of Peptic Ulcers: When relieves pain associated with Duodenal ulcers occur?

A

Relieved by food or antacids

158
Q

Types of Peptic Ulcers: In duodenal ulcers, increased acid load is caused by?

A

Increased acid load caused from H. pylori

159
Q

What does H.pylori do in Duodenal ulcers?

A

H. Pylori activates immune cells (T&B lymphocytes), cytokines, neutrophils –> damages mucosa

160
Q

How do Duodenal ulcers heal?

A

Heal spontaneously but reoccur

161
Q

Types of Peptic Ulcers: Gastric ulcers (stomach ulcers)
What are they?

A

A lesion in mucosal wall of stomach breaks down mucosal barrier

Permits H+ ions –> mucosa –> Disrupts cell structure

162
Q

Where else can gastric ulcers be seen?

A

Less freq, more deadly, chronic, can be seen in chronic gastritis

163
Q

What are gastric ulcers seen in chronic gastritis more likely to result in?

A

more likely to result in obstruction, & increase cancer risk

164
Q

What does histamines do in gastric ulcers?

A

Histamine released from the damaged mucosa –> vasodilation and increased capillary permeability –> further secretion of acid and pepsin.

165
Q

What can gastric ulcers do to the stomach wall?

A

Can perforate stomach wall  gastric contents enter abdominal cavity

166
Q

What makes pain worse in gastric ulcers?

A

Pain worse when eating –> anorexia

167
Q

What are stress ulcers?

A

Major physiological stressor

severe illness or major trauma

168
Q

What can cause stress ulcers?

A

Due to local tissue ischemia (HF, sepsis, burns, shock, anoxia, sympathetic responses)

169
Q

Complications of all peptic ulcers include?

A

Complications – GI hemorrhage (hematemesis or melena), obstruction, perforation (destruction of multiple layers), peritonitis, gastric ca

170
Q

Defense factors of the stomach against H.pylori?

A

Mucus
Bicarbonate
Blood flow
Prostaglandins

171
Q

What is bicarbonate secreted from?

A

Secreted by epithelial cells of stomach and duodenum

172
Q

What is bicarbonate produced by?

A

Produced by pancreas, secreted into lumen of duodenum

173
Q

What does bicarbonate do?

A

Neutralizes acids

174
Q

What happens to blood flow is poor in the stomach?

A

Poor blood flow –> ischemia, cell injury, and vulnerability to attack by acid/pepsin

175
Q

What do prostaglandins stimulate? What does it promote?

A

Stimulate the secretion of mucus and bicarbonate, promote vasodilation, maintains submucosal blood flow, suppress gastric acid

176
Q

Patho of PUD: What are aggressive factors leading to PUD?

A

H Pylori
NSAIDs
Gastric Acid
Pepsin
Smoking

177
Q

What do NSAIDs inhibit?

A

Inhibit PGs

178
Q

Because NSAIDs inhibit prostaglandins, what does this lead to (having to do with PUD)?

A

Decrease submucosal blood flow
Suppress mucus/bicarb
Promote gastric acid
Irritant

179
Q

What does gastric acid do in PUD?

A

Injures cells of GI mucosa, activates pepsin

180
Q

What does pepsin do in PUD?

A

Proteolytic enzyme in gastric juice
Injures gastric mucosa

181
Q

What does smoking do in PUD?

A

Delays healing, vasoconstriction

182
Q

Why does Heartburn & acid regurgitation
occur in GERD?

A

Chyme periodically backs up from the stomach into the esophagus.

Reflux of bile salts, acid and pepsin from the stomach to the esophagus compromises its defenses causing esophagitis, inflammation, ulceration, precancerous lesions (Barrett esophagus)

183
Q

Gastroesophageal reflux disease (GERD)- what is it?

A

Heartburn & acid regurgitation

184
Q

What would cause GERD?

A

Abnormalities in LES function, esophageal & delayed gastric motility

185
Q

What does GERD eventually lead to?

A

Eventually, fibrosis and strictures develop in the esophagus.

186
Q

What occurs in GERD that would lead to dysphagia and weightloss?

A

Edema, strictures, esophageal spasms, decreased esophageal motility –> dysphagia/wgt loss

187
Q

What has little to no role in GERD?

A

H. pylori has little to no role

188
Q

Common predisposing factors to GERD?

A

Hiatal hernia
Delayed gastric emptying
Vomiting
Coughing
Lifting, bending
Constipation
Foods

189
Q

Look at slide 36

A

gastroparesis

190
Q

What can foods cause that lead to GERD?

Foods like what?

A

chocolate, peppermint, fatty foods, coffee, and tea decrease lower esophageal sphincter (LES) pressure, predisposing to reflux

191
Q

What do acidic foods do to cause GERD? Like what?

A

Acidic foods, such as tomato-based products, orange juice, cola, and red wine, may irritate the esophagus.

192
Q

What are common causes of GERD?

A

There is no single cause for GERD.
Incompetent LES:

lower esophageal sphincter (LES)

193
Q

What does lower esophageal sphincter (LES) do to cause GERD?

A

An incompetent LES lets gastric contents reflux from the stomach to the esophagus when the patient is supine (lying down on back).

194
Q

What are clinical manifestations of GERD?

A

Heartburn/Pain/Dyspepsia

Regurgitation

195
Q

What is included in heartburn/pain/dyspepsia?

A

Burning or tight sensation in the chest –> jaw

196
Q

When does Heartburn/Pain/Dyspepsia
associate with GERD occur?

A

Usually occurs 60 minutes after eating

Worse at night, rousing from sleep

Sx worse with increased intra-abd pressure

Pain or discomfort centered in the upper abdomen.

197
Q

Regurgitation in GERD

A

Hot, bitter, or sour liquid coming into the throat or mouth. This sour taste in the mouth occurs after meals.

198
Q

What are treatments for GERD?

A

Tx: PPIs, H2RAs, antacids, prokinetics

199
Q

Non-Pharm Management for GERD

A

Smoking cessation
Weight loss
Elevating head of bed
Meal patterns & timing
Avoidance of trigger foods/beverages

200
Q

Non-Pharm Management for GERD

A

Increased fluid intake with food consumption alone not adequate
Increase consumption of protein-rich diet
Clothing ~ loose
Proper administration of irritating medications ~ remain upright & plenty H2O
Symptom diary

201
Q

How should meals be with GERD?

A

Avoid 2-3h of bedtime/sleep
Smaller meals

202
Q

What foods/beverages should be avoided with GERD?

A

Alcohol
Caffeine, chocolate, peppermint
Dietary fat intake
Citrus, oranges, tomatoes, onions & spicy foods, carbonated beverages

203
Q

Classes of Antiulcer Drugs

A

Antibiotics
Proton Pump Inhibitors
Histamine2 Receptor Antagonists/Blockers
Gastric Lumen Adherent Cytoprotectives
Antisecretory agents that enhance mucosal defenses
Antacids

204
Q

Proton Pump Inhibitors PPIs (What do they end in). What are the prototypes?

A

“zole”

Prototype: Omeprazole (Prilosec), Pantoprazole (Protonix)

205
Q

What are the most effective drugs for suppression of gastric acid? What do they do?

A

PPIs

Most effective drugs for suppression of gastric acid, reduce gastric acid by 90%

Fast acting

206
Q

What is the mode of action of Proton Pump Inhibitors? Where do they work?

A

Works in parietal cells of stomach

207
Q

What is the mode of action of Proton Pump Inhibitors? What do they inhibit?

A

Irreversible inhibition of H+,K+-ATPase (proton pump)

208
Q

H+,K+-ATPase (proton pump) - what does it do?

A

This is the enzyme that produces gastric acid

209
Q

How are Proton Pump Inhibitors PPIs metabolized and excreted?

A

Hepatic metabolism, renal excretion

210
Q

How long is the half life, how long do effects persist of Proton Pump Inhibitors PPIs ?

A

½ life 1 hr but effects persist long after drug leaves body

211
Q

What do PPIs have to protect against the stomach coating?

A

Protective EC coated to protect from stomach acid

212
Q

How is Pantoprazole administered?

A

Pantoprazole – PO, IV push, IV drip for GIB

213
Q

How are Proton Pump Inhibitors PPIs used?

A

Short-term tx of PUD, erosive esophagitis, GERD

214
Q

How long should Proton Pump Inhibitors PPIs be used?

A

Limit tx to 4-8wks

215
Q

Proton Pump Inhibitors PPIs work more effectively and faster than what?

A

More effective & faster than H2RAs

216
Q

What do Proton Pump Inhibitors PPIs prevent?

A

Prevent stress ulcers

217
Q

Minor adverse effects of Proton Pump Inhibitors PPIs?

A

Minor: GI ~ n/v/d, CNS ~ headaches, dizziness

218
Q

Major adverse effects of Proton Pump Inhibitors PPIs?

A

Major: Pneumonia, osteoporosis, acid rebound upon d/c, HypoMg/Ca by reducing intestinal absorption (↑risk w/diuretics), C.diff

219
Q

What should you teach patients to report immediately with Proton Pump Inhibitors PPIs use?

A

Teach pts to report diarrhea immediately

220
Q

Nursing Implications of PPIs: How should patient take PPI capsules/tablets?

A

Capsules & tablets should be swallowed intact, not crushed, split or chewed

221
Q

Nursing Implications of PPIs: When should PPIs be taken?

A

Depending on PPI may be taken at least an hour to right before meals or just before eating.

Some PPIs taken w/o regard to food

222
Q

Nursing Implications of PPIs: How are the risks v benefits of PPI use?

A

Risks > Benefits LT use

223
Q

Nursing Implications of PPIs: What should you warn patients about with PPI use?

A

Inform pts about s/sx of resp infection

224
Q

Nursing Implications of PPIs: What should you encourage patients to maintain while taking PPIs?

A

Encourage pts to maintain adequate Ca & Vit D intake

225
Q

Nursing Implications of PPIs: How should patients avoid acid rebound?

A

Advise pts that acid rebound can be minimized by using lowest dose for shortest time.

226
Q

Nursing Implications of PPIs: How should patients manage symptoms?

A

Sx may need to be managed w/H2RA & antacids

227
Q

Nursing Implications of PPIs: What should you warn patients about?

A

Inform pts about risk of hypoMg (tremors, muscle cramps, seizures, dysrhythmias)

228
Q

Nursing Implications of PPIs: What levels may be increased with PPI use?

A

Serum levels of Digoxin may be slightly increased

229
Q

Histamine2 Receptor Antagonists (H2RAs): What is the prototypes?

A

Prototype: Cimetidine (Tagamet), Famotidine (Pepcid), Ranitidine (Zantac)

230
Q

Histamine2 Receptor Antagonists (H2RAs) MOA: How do histamines act?

A

Histamine acts through two types of receptors named H1 and H2

231
Q

Histamine2 Receptor Antagonists (H2RAs) MOA: When histamine stimulates H2 receptors, what happens?

A

H2 receptors on parietal cells stimulated by histamine –> promote gastric secretion

232
Q

Histamine2 Receptor Antagonists (H2RAs) MOA: When H2RAs block H2 receptors, what happens?

A

H2RAs block H2 receptors —> decreased gastric acid secretion & H+ ion concentration

233
Q

Histamine2 Receptor Antagonists (H2RAs): Is it selective or nonselective?

A

Selective blockade of H2 receptors

234
Q

What is the pk of Histamine2 Receptor Antagonists (H2RAs)?

A

PKs: varies by prototype

235
Q

How should Histamine2 Receptor Antagonists (H2RAs) be taken? Administration, dose, freq, route?

A

Administration, dose, frequency, route varies by prototype
May be taken without regard to meals

236
Q

What is Histamine2 Receptor Antagonists (H2RAs) used for?

A

Gastric & duodenal ulcers treatment, healing, prophylaxis

GERD

237
Q

What does ADR of Histamine2 Receptor Antagonists (H2RAs) depend on?

A

ADRs (depend on prototype)

238
Q

ADRs of Histamine2 Receptor Antagonists (H2RAs) depend on prototype and include?

A

Pneumonia (elevation of gastric pH)
Stomach candida

239
Q

Drug interactions of Histamine2 Receptor Antagonists (H2RAs)

A

Vary per prototype

240
Q

Nursing Implications of H2RAs: How should they be taken?

A

Most H2RAs may be taken without regard to meals

241
Q

Nursing Implications of H2RAs: When is it best to take H2RAs?

A

Dosing is @QHS for better suppression of nocturnal acid secretion or BID

QHS= once per day at bed time.

BID= twice per day

242
Q

Nursing Implications of H2RAs: What should you educate patients about?

A

Educate pts about s/x GIB

Black tarry stools, coffee-ground emesis
  Tx should increase gastric pH > 5 & pain relieved
243
Q

Nursing Implications of H2RAs: What should you warn patients about?

A

Inform pts about s/sx of resp tract infection

244
Q

Nursing Implications of H2RAs: How should you take antacids?

A

Separate from antacids by at least 1 hr
Absorption may be decreased

245
Q

Sucralfate [Carafate]- What does it do?

important

A

Creates a protective barrier against acid/pepsin for up to 6 hours

246
Q

Sucralfate [Carafate]. Creates a protective barrier against acid/pepsin for up to 6 hours- How?

A

Forms a viscid sticky gel & adheres to ulcer crater

247
Q

Sucralfate [Carafate].- What does it NOT do?

A

Does not decrease acid secretion/no acid neutralizing capability

248
Q

Sucralfate [Carafate].-Therapeutic uses?

A

Acute ulcers and maintenance therapy

249
Q

PKs of Sucralfate [Carafate].-absorption and excretion?

A

Adm orally, minimal systemic absorption
90% of each dose eliminated in feces

250
Q

Sucralfate [Carafate]- adverse effects?

A

Constipation (only 2% of patients)

251
Q

Sucralfate [Carafate]- how can it be taken?

A

Tx 4-8 wks

Can be halved, broken, or dissolved in 15-30mL H2O to form a slurry
Tablets do not crush well, but you may try splitting tablets.

252
Q

Sucralfate [Carafate]- Drug interactions

How should antacids be administered with this med? Why?

A

Antacids may interfere with effects of sucralfate by raising gastric pH >4

Adm 30 min apart

253
Q

Sucralfate [Carafate]- Drug interactions
may impede absorption of some drugs- what does that mean?

A

May impede absorption of some drugs, so adm 2h apart

254
Q

Misoprostol (Cytotec): MOA- what is this med a replacement for?

A

MOA: Replacement for endogenous prostaglandins

255
Q

Misoprostol (Cytotec): Uses of med

A

Uses: prevention of gastric ulcers caused by LT NSAID tx

256
Q

Misoprostol (Cytotec): ADRs?

A

diarrhea, abdominal pain

257
Q

Misoprostol (Cytotec): Contraindicated in?

A

Contraindicated in pregnancy

258
Q

Misoprostol (Cytotec): Why is it Contraindicated in pregnancy?

A

PGs stimulate uterine contractions

Can cause partial/complete expulsion of developing fetus

Women if childbearing age must comply with birth control, be advised on dangers, & have neg pregnancy test within 2 weeks before beginning tx

259
Q

Misoprostol (Cytotec): What must women of child bearing age have before starting med?

A

Women if childbearing age must comply with birth control, be advised on dangers, & have neg pregnancy test within 2 weeks before beginning tx

260
Q

COmbinations of Antacids available?

(Start with aluminum hydroxide)

A

Aluminum hydroxide + magnesium hydroxide + simethicone (Mylanta)

Aluminum hydroxide + magnesium hydroxide (Maalox)

261
Q

Combinations of Antacids available?
(Last 2 not including Aluminum hydroxide)

A

Calcium Carbonate (Tums)
Sodium bicarbonate (Alka-Seltzer)

262
Q

What are antacids used for?

A

Used for hyperacidity, indigestion, reflux

263
Q

Antacids are available in suspensions and tablets, how should they be taken in these forms?

A

Suspensions - shake well
Chew tablets thoroughly, then H2O or milk

264
Q

What kind of tablets are Antacids?

A

Effervescent tablets

Effervescent tablets are designed to release carbon dioxide upon contact with water, promoting their disintegration.

265
Q

How should antacids be taken?

A

Taken regularly, not PRN

266
Q

How should dosing of antacids be? Why?

A

Short duration of action = frequent dosing

267
Q

What kind of compounds are antacids? What does this mean they do?

A

Alkaline compounds that neutralize stomach acid

Reduce destruction of gut wall

268
Q

What are antacids used for?

A

Uses: PUD, sx of GERD (no studies demonstrate efficacy)

Can provide prophylaxis against stress-induced ulcers & symptomatic relief, but they do not accelerate healing.

269
Q

How do antacids effect stomach pH?

A

Except for sodium bicarbonate, antacids do not alter systemic pH

270
Q

What has antacid use been replaced by?

A

H2RAs & PPIs

271
Q

Who should use antacids cautiously?

A

Use with caution in patients with renal impairment

272
Q

Adverse effects of antacids?

A

Constipation: Aluminum hydroxide
Diarrhea: Magnesium hydroxide
Combinations can minimize bowel effects (Maalox)

Sodium loading
-Caution with HF

273
Q

What are adverse effects of antacids with Aluminum hydroxide

A

Constipation

274
Q

What are adverse effects of antacids with Mg hydroxide

275
Q

Drug interactions (due to increased pH)
in antacids would occur why?

A

(due to increased pH)

276
Q

Drug interactions (due to increased pH)
Antacids:

A

Elevation of urinary ph can excrete acidic drugs & delay excretion of basic drugs

277
Q

The ADRs of antacids for drugs interactions means what?

A

Allow at least 1 between antacids and other meds (eg ASA)

278
Q

Antacids: Magnesium Hydroxide [Milk of Magnesia]- what is the most prominent adverse effect?

A

Most prominent adverse effect is diarrhea

279
Q

What is Magnesium Hydroxide usually taken with?

A

aluminum hydroxide

280
Q

Who should Magnesium Hydroxide [Milk of Magnesia] be avoided in?

Who should it be used cautiously in?

A

Avoided in patients with undiagnosed abdominal pain
Stimulation of bowel could be dangerous

Use with caution in patients with renal failure- Mg can accumulate to toxic levels (eg CNS depression)

281
Q

Aluminum Hydroxide- what does it do?

A

Binds to pepsin, which may facilitate healing

282
Q

Antacids: What does Aluminum Hydroxide bind with?

A

Binds with phosphate

283
Q

When Aluminum Hydroxide binds with phosphate, what does it cause?

A

Reduce absorption & cause hypophosphatemia

284
Q

What does Aluminum Hydroxide drug interactions include? What would binding effects be?

A

Tetracyclines, warfarin, digoxin
Binding may reduce their effects

285
Q

Calcium Carbonate (Tums)- What do they act as? How long is their duration of action

A

Also acts as calcium-based phosphate binder

Long duration of action

286
Q

Principle adverse effects of calcium carbonate (Tums)

A

Principal adverse effect: Constipation, which can be overcome by combining calcium carbonate with a magnesium-containing antacid (eg, magnesium hydroxide)

287
Q

Rare side effect of calcium carbonate?

A

Milk-alkali syndrome

288
Q

Milk-alkali syndrome

A

Condition characterized by hyperCa++, met alk, soft tissue calcification, impaired renal function
Taking too many calcium supplements or chronic ingestion

289
Q

Who should calcium carbonate be used cautiously in?

A

Caution with renal patients (e.g calcium & phosphate levels)

PATHO/PHARM II (27 decks)

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