Ingestive Medications

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created 1 year ago by Keilana_N
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GI Tract
updated 1 year ago by Keilana_N
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pharmacology
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1

Purpose of pH

  • breakdown of food especially proteins
  • protection against bacterial invasion
2

1mm

size of food to pass out of stomach through pyloric valve

3

Stomach protected from acid by

  • mucus layer
  • epithelial cell layer
  • brunner glands
  • blood flow
  • prostaglandins
4

Cardiac portion:

Esophagus protected from acid backflow by lower esop sphincter (LES)

high pressure zone (HPZ)--> protection

5

Cardiac gastric glands located here

Cardiac portion: secrete mucus --> protection

6

Fundus of stomach [FUS]

Gastric glands location

composed of:

parietal, chief, mucous/surface epithelial/mucous neck cells

7

Parietal

  1. HCl production
  2. Produce and secrete hydrochloric acid
  3. Primary site for acid-blocking medications
  4. Located throughout length of gland
8

Parietal cells are stimulated by __________, __________, and _________ binding to its surface receptors.

  • histamine
  • acetylcholine
  • gastrin
9

Occupation of receptor sites after binding sends second message into cell to produce HCL

  1. Histamine produces cAMP through a series of steps and cAMP provides energy to the proton pump that then transports hydrogen ions to make HCl
    1. Histamine receptor antagonists (H2 receptor antagonists; H2RA)
  2. Acetylcholine and gastrin bind with receptors to activate the proton pump (PP) through calcium that then produces HCl acid
    1. Inactivation of proton pump occurs with proton pump inhibitors (PPI)
10

HCL acid production stimulated through

  • sight
  • smell
  • taste of food
  • presence of food in stomach
11

Chief cells

Secretes pepsinogen (proenzyme) that changes to pepsin (activated) when exposed to acid
1. Located at base of gland
2. Normally breaks down proteins into peptides

12

Anything that stimulates production of HCL in chief cells leads to:

secretion of pepsinogen (so need to block HCl acid)

13

Mucous/surface epithelial/mucous neck cells

Secrete mucus to protect stomach lining from HCL

14

If mucus layer is disrupted, then increased risk for

damage from HCl acid (medications especially NSAIDs and steroids disrupt mucus blanket)--> PUD or abdominal pain

15

Submucosal blood flow may decrease with

  • Age
  • Disease
16

Without ___________ healing of mucus layer cannot __________

blood flow; occur quickly

17

If mucus layer damaged and inadequate blood flow result to:

increases risk for damage to gastric lining

18

Prostaglandins

  • Protective
  • Normally stimulate secretion of mucus and HCO3
  • Increase vasodilation-->increase blood flow
19

Interference with prostaglandins increases risk for

damage to gastric mucosa (NSAIDS interfere with prostaglandins)

20

GERD/gastroesophageal reflux disease

LES incompetence

21

GERD affected by:

  • alcohol ETOH
  • caffeine
  • chocolate
  • Calcium channel blocker medications (CCB)
  • peppermint/mints
  • spicy foods
22

two types of GERD

Erosive and non-erosive

23

Erosive type of GERD cause

breaks in mucosa of esophagus

24

Other risk for GERD

esophageal cancer due to Barrett’s epithelium

ECBE

25

Cannot improve LES pressure in GERD, so provide

medication to decrease acidity in stomach -->less acid refluxed into esophagus

26

GERD Nursing care

  1. Avoid foods that increase reflux such as: chocolate, peppermint, caffeine, high fat foods, spicy foods;
  2. upright for 2 hours after eating
  3. no food for 2 hours before bedtime
  4. small frequent meals
  5. avoid overeating
  6. elevate HOB
27

Peptic Ulcer Disease (PUD) caused by:

Helicobacter pylori (H. pylori)

28

Age and percentage greatly affected by PUD

Over Age 60; 40-60%

29

PUD found on younger adults age and percentage

Under Age 30; 10%

30

PUD gray area age between

30-60 years

31

Helicobacter pylori (H. pylori)

lives between the mucus layer and the epithelial layer lining the stomach so it is protected from acidity of the stomach

32

90% of H. Pylori is responsible and positive for this disease

Duodenal Ulcers (DU)

33

70% of H. Pylori is responsible and positive for this disease

Gastric Ulcers (GU)

34

True or False: H. pylori also present in many who do NOT have PUD

TRUE

35

plays a role in gastric cancer since Mucosa Associated Lymphoid Tumor (MALT) regresses when this organism eradicated (60-90% regress)

H. pylori

36

PUD Nursing Care

  1. Teach patient antibiotic is required to eradicate H. Pylori if patient is positive for bacteria; will also take H2RA or PPI
    1. Risk is people who self-medicate and sx return since bacteria is not eradicated
37

PUD: Assessment/cues:

change in eating pattern; assess pain pattern, any prior GI surgery or diseases

38

PUD Plan/Implement:

Teach med actions, side effects, no need to change diet, disease process; need to take all of medication

39

PUD Pro-kinetic agent

Metoclopramide/Reglan

40

Metoclopramide/Reglan Action:

increase tone and motility of GI tract

41

Metoclopramide/Reglan Indications

Gastroesophageal reflux disease/GERD; chemotherapy induced nausea and vomiting/CINV and diabetic gastroparesis; facilitation of small bowel intubation or radiologic examination of GI tract

42

Metoclopramide/Reglan Adverse Effects

  • high dose therapy - sedation and diarrhea
  • long term high dose therapy -tardive dyskinesia with repetitive, involuntary movements of arms, legs and facial muscles (older adults especially vulnerable)
43

Metoclopramide/Reglan Nursing Care:

Look at why patient ordered the med and determine actions from there. If gastroparesis and problems with gastric emptying, teach small frequent meals, low fat diet, stay upright for 2 hours after eating; If indication is CINV, then nursing monitors fluid balance

44

Stress-Related Ulcers (SRU)

Common in ICU population

45

SRU Multi-factorial - decreased blood flow -->

  • Mucosal ischemia
  • Reperfusion injury
  • head injury causing increased acid production
46

SRU Risks

  • Many different procedures (N/G, vents others)
  • Coagulopathy (abnormalities in blood especially clotting factors)
  • History of PUD or GI bleed
  • Sepsis and Systemic Inflammatory Response Syndrome (SIRS)
  • Use of steroids (such as prednisone) that decrease immune functioning
  • ICU stay greater than 1 week
  • Occult bleeding
47

SRU interventions

Preventive use of medications in critically ill common

48

Types of anti-acid medications

  • Antacids (OTC)
  • H2 receptor antagonists/H2RA
  • Proton Pump Inhibitors/PPI
  • Misc: Sucralfate, Misoprostel
49

Antacids (over the counter=OTC)

  • Neutralize stomach acid via aluminum, magnesium, calcium &/or sodium salts
  • Available in combination salts
50

Act through neutralizing acid by stimulating production of mucus (protective barrier), prostaglandins (prevent histamine from binding with parietal cell receptor) and bicarbonate (HCO3) (buffers acid)

Antacids (over the counter=OTC)

51

Types of Antacids (OTC)

  • Magnesium based: MOM
  • Aluminum based: Basaljel, alternajel, amphogel (all contain significant sodium)
  • Combination Al and Mg: gaviscon, Maalox, Mylanta, DiGel
    1. Attempt to control side effects
  • Calcium containing: Tums, Maalox caplets, extra strength Alkets
  • Sodium containing: Alka-Seltzer
52

Magnesium based Antacid

Milk of Magnesia (MOM)

53

Aluminum based Antacid

Basaljel, alternajel, amphogel (all contain significant sodium)

note: suffix jel,gel

54

Combination Al and Mg antacids that attempts to control side effects

  • DiGel
  • Gaviscon
  • Maalox
  • Mylanta

DGMM

55

Calcium containing antacids are:

  • Alkets (extra strength)
  • Maalox caplets
  • TUMS
56

Sodium containing antacids are:

Alka-Seltzer

57

Antacids adverse effects

  1. Magnesium based (MOM)- diarrhea
  2. Aluminum and calcium based- constipation
  3. Calcium products- kidney stone risk though not significant
  4. Rebound hyperacidity
  5. Milk-alkali syndrome/calcium alkali syndrome
58

TRUE OR FALSE: Rebound hyper-acidity risk on all antacids and more common with calcium containing products

TRUE

59

How to stop hyper-acidity with antacids?

Tapering off may help

60

Milk-alkali syndrome/calcium alkali syndrome

not common but is a combination of

  • hyperchloremic alkalosis
  • impaired renal function
  • soft tissue calcifications
61

Increased blood calcium levels due to excessive intake of calcium and alkali results to:

Milk-alkali syndrome/calcium alkali syndrome

62

OTC Treatment for milk-alkali syndrome/calcium alkali syndrome

TUMS for osteoporosis often in addition to calcium tablets

63

RISK for Milk-alkali syndrome/calcium alkali syndrome

is renal damage --> failure

64

All interactions of antacids is based on

ability to bind with another medication

65

Antacids interaction outcomes include:

  • interfering with absorption = insoluble complex (no absorption),
  • increased stomach pH = increased absorption of alkaline meds
  • decreased absorption of acid meds
  • increases excretion of acidic meds
  • Increased urinary pH = decreased elimination of base meds
66

H2 receptor antagonists/H2RA

Reduce acid secretion but do not eliminate it

  1. Recall acid stimulated by histamine, acetylcholine and gastrin
67

Examples of H2RA

  • cimetidine/Tagamet
  • ranitidine/Zantac
  • famotidine/Pepcid
  • nizatidine/Axid
  • NOTE: suffix "dine"
68

ACTION of H2 receptor antagonists/H2RA

Block histamine receptor (H2) on parietal cell-->blocks production of cAMP energy that normally fuels proton pump (that makes HCl Acid) = decreases about 65% of acid in stomach and increases pH of stomach

69

Decreases about 65% of acid in stomach and increases pH of stomach

H2 receptor antagonists/H2RA

70

H2 receptor antagonists/H2RA use/indications

  • GERD
  • PUD
  • Erosive esosphagitis
  • Erosive gastroesophageal disease/GERD
  • Adjuctive treatment for UGI bleeding
  • Stress ulcer prophylaxis
  • Pre-operatively to prevent aspiration pneumonitis during anesthesia
    • Given 60-90 minutes before surgery
71

Adverse Effects of H2 receptor antagonists/H2RA

  • Less than 3% BUT all side effects more likely with cimetidine
  • Older adults susceptible to CNS changes of confusion and disorientation
72

CV Adverse Effects of H2 receptor antagonists/H2RA

  • hypotension
  • dysrhythmias (especially if IV infusion)
73

CNS Adverse Effects of H2 receptor antagonists/H2RA

HA, lethargy, confusion depression, hallucinations, slurred speech, agitation (all more likely in elderly); medication crosses blood brain barrier (BBB)

74

ENDO Adverse Effects of H2 receptor antagonists/H2RA

increased prolactin secretion -->gynecomastia (likely with cimetidine since it binds with androgen receptors-no binding with other meds)

75

GI Adverse Effects of H2 receptor antagonists/H2RA

diarrhea, nausea, abdominal cramps

DNA

76

GU Adverse Effects of H2 receptor antagonists/H2RA

impotence (cimetidine)

increased BUN

increased serum creatinine

77

H2 receptor antagonists/H2RA - Nursing Care

increased risk for pneumonia due to increase in ph (pathogens are not killed by acid)

78

Proton Pump Inhibitors/PPI

Binds hydrogen-potassium-ATPase pump--> inhibits enzyme--> total blockage of H+ secretion from parietal cells.

  • One dose decreases acid production by 97% within 2 hours.
  • Effects last 24 hours because it takes the body that long to re-build the proton-pump
79

Examples of Proton Pump Inhibitors/PPI

  • lansoprazole/Prevacid
  • omeprazole/Prilosec
  • pantoprazole/Protonix
  • esomeprazole/Nexium
  • rabeprazole/Aciphex
  • dexlansoprazole/Dexilant
80

Dexlansoprazole/Dexilan

dual delayed release for medication release in proximal and again in distal small intestine

81

Esomeprazole

believed to achieve higher blood levels with longer effects

82

Rabeprazole/aciphex

has some antibacterial properties

83

Function of pump in PPI

to transport hydrogen ions out of parietal cell--> increase gastric acid and lower pH.

  • PPI meds then bind to the proton pump and pump cannot function
84

PPI meds stop more than ___% of acid secretion for _______ hours.

90; 24

85

Achlorhydria

risk of bacterial overgrowth, intestinal metaplasia (aberrant cells), lack of intrinsic factor (needed to absorb vitamin B12 and requires acid environment), and hip fractures due to decreased absorption of calcium

86

PPI indications

  1. Erosive esophagitis, symptomatic GERD, active duodenal ulcers, NSAID-induced ulcers, hypersecretory states, stress ulcer prophylaxis
  2. Useful with antibiotics for H.pylori infections
87

PPI adverse effects

  1. Well tolerated overall
  2. Headache/HA, diarrhea, nausea, flatus and dry mouth may occur
  3. Concern for increased risk for fractures thought related to osteoporosis
  4. Clostridium Difficile/C diff infections, and depletion of magnesium (symptoms are tremors, muscle cramps, dysrhythmias and seizures)
  5. Rebound hyperacidity possible with discontinuing medication so taper is suggested
88

Long-term use of PPI increases the risk for _______. Hence, short-term use only recommended.

renal failure

89

Sucralfate

  1. Action is local to bind directly onto surface of ulcer
  2. Once exposed to stomach acid, it dissociates into aluminum hydroxide and sulfate anions
  3. Not used commonly due to transient effects and multiple daily dosing (every 6 h)
  4. Adverse: few: nausea, constipation, dry mouth
  5. Given 1 hour before meals & bedtime
90

Aluminum salt in sucralfate stimulates production of

mucus and HCO3-->sticky viscid gel that adheres to ulcer site for up to 6 hours

91

Sulfated sucrose molecules bind to _________________ forming protective barrier --> limits access of pepsin

positively charged tissue proteins at base of ulcer

92

Stimulates secretion of prostaglandins that are protective

Sucralfate

93

Misoprostel

  1. Prostanglandin E analogueàthought to inhibit gastric acid secretion
  2. Also believed to protect mucosa from injury (cytoprotective) by helping mucus production or bicarbonate, promotes local cell regeneration and helping maintain blood flow through mucosa (see action of prostaglandins earlier)
  3. Thought to be useful to decrease incidence of ulcers when taking NSAIDS but require large dosages that may produce diarrhea and abdominal cramps
94

Misoprostel Adverse Effects

Headache/HA, GI distress, vaginal bleeding

95
  1. In U.S. only approved for prophylaxis but is given for GI acidity problems and protection in other countries
  2. Not for pregnant women or anyone desiring pregnancy since causes uterine contractions and expulsion of fetus

Misoprostel

96

Vitamins

organic molecules used by body for growth or repair of tissue

97

Minerals

inorganic substances found normally in earth

98

Enzymes

proteins secreted by cells that cause a change in another substance

99

Co-Enzymes

may enhance or is necessary for an action by an enzyme

100

Recommended Daily Allowance/RDA:

required minimum daily needs of essential nutrients

101

Types of Vitamins

water soluble and fat soluble

102

Water soluble vitamins

B complex group and Vitamin C

103
  • may be dissolved in water
  • easily excreted
  • are not stored in body (except vitamin B12) therefore, daily intake required

Water soluble vitamins: B complex group and Vitamin C

104

Examples of B Vitamins

B1/thiamine

B2/riboflavin

B3/niacin

B5/pantothenic acid

B6/pyridoxine

B7/biotin

B9/folic acid

B12/cyanocobalamin

105

B1/thiamine deficiency

beriberi (wet form and dry form) or cerebral form of beriberi that may be seen in alcoholic is Wernicke-Korsokoff Syndrome/wernicke encephalopathy

106

B1/thiamine Symptoms of deficiency:

  • effusions
  • CNS lesions
  • polyneuropathy
107

Action of thiamine:

precursor that ultimately plays a role in the Kreb’s cycle that is needed for CHO metabolism, key role in PNS integrity, CV system and GI tract

108

Source of thiamine

whole enriched grain & flour

109

adverse effects of thiamine

rare (water soluble); hypersensitivity reactions, n, restlessness, pulmonary edema, pruritus, urticarial, weakness, sweating, angioedema, cyanosis, CV collapse

110

Banana bag

Important in alcoholic patients due to risk of Wernicke-Korsokoff Syndrome if glucose given without thiamine

111

B2/riboflavin deficiency

cheilosis/angular stomatitis, seborrheic dermatitis and keratitis

112

B2/riboflavin action

converted into two enzymes needed for tissue respiration; role in CHO catabolism, needed to activate vitamin B6 (pyridoxine)

113

B2/riboflavin source

primarily dairy products; Note: riboflavin inactivated by light so milk should not be in a clear glass container; yogurt, cheese, milk, enriched breads and cereals, whole grains

114

B3/niacin deficiency

pellagra

crusting, erythema, and desquamation of skin, scaly dermatitis (especially areas exposed to sun), inflammation of oral cavity (includes glossitis), vaginal and urethral mucosa, diarrhea, bloody diarrhea, psychotic disorders

115

B3/niacin action

due to metabolic product called nicotinamide—needed for CHO, protein, purine and lipid metabolism and tissue respiration; needed for glycogenolysis

  1. May decrease cholesterol levels but need high doses likely to cause extreme flushing and tachycardia
116

B3/niacin source

Enriched breads, milk, meat, poultry, fish, potatoes, liver

117

B3/niacin adverse effects

flushing, pruritus, GI distress

118

B5/pantothenic acid

  1. No clear evidence of use but used for variety of conditions
119

Believed to be essential part of coenzyme A and acyl carrier proteins; coenzyme A needed for gluconeogenesis, intermediary metabolism of carbohydrates/CHO, synthesis of steroids, hormones and acetylcholine

B5/pantothenic acid

120

B5/pantothenic acid source

broccoli

chicken

egg yolk

peanuts

whole grains

121

B6/pyridoxine deficiency

anemia, neurologic disturbances, seborrheic dermatitis, cheilosis/angular stomatitis, formation of xanthine stones (rare) in urine; peripheral nerves effected, skin and mucous membrane changes, seizures in neonates and infants

122

composed of 3 compounds all of which are converted to coenzymes in RBC

B6/pyridoxine

123

B6/pyridoxine action

protein, CHO and lipid use in body, important role in conversion of tryptophan (AA) to niacin (B3) and serotonin(neurotransmitter), essential in production of GABA (neurotransmitter in CNS), important in synthesis of heme and maintenance of hematopoietic system, needed for integrity of peripheral nerves, skin and mucous membranes

124

B6/pyridoxine source

  • eggs
  • chicken
  • cereals
  • fish
  • pork
  • whole grains
125

B6/pyridoxine adverse effects

rare and then usually if large doses over long time with neurotoxicity most likely to occur

126

B7/ biotin deficiency

alopecia, scaly, erythematous (red) rash around eyes, nose, mouth, genitalia

127

B7/ biotin action

metabolize CHO, fats and amino acids, vital for growth of fetus

128

B7/ biotin source

  • egg yolks
  • nuts
  • peanut butter
  • yeast
129

B9/folic acid deficiency

  • neural tube defects
  • anemia
  • lethargy
  • fatigue
  • pale skin
  • weakness
130

B9/folic acid (folate=natural form and folic acid is synthetic) action

vital to DNA and development of neural tube in fetus (actually develops day 21-28 so may be before woman knows she is pregnant)

131

essential for DNA synthesis therefore deficiency of either leads to megaloblastic anemia (large RBC)

Folic acid and B12

132

B9/folic acid source

  • bananas
  • bread
  • enriched cereal
  • flour
  • Green leafy vegetables
  • melons
  • organ meat
133

B12/cyanocobalamin deficiency

  • pernicious anemia
  • weakness
  • numbness & tingling hands and feet
  • difficulty walking
  • weight loss
  • irritability
  • diarrhea
  • tachycardia
134

B12/cyanocobalamin action

DNA synthesis, fat and CHO metabolism and synthesis of protein, growth, cell replication, hematopoiesis, myelin synthesis (any cells with rapid replication)

135

Requires exogenous source as well as intrinsic factor

B12/cyanocobalamin

136

B12/cyanocobalamin source

  • animal origin
  • intrinsic factor - required from stomach
137

B12/cyanocobalamin synthetic advised for anyone in the age of

> 50

138

B12/cyanocobalamin adverse effects

  • diarrhea
  • fever
  • itching
  • nontoxic
139

Example of C Vitamin

Ascorbic acid

140

Vitamin C/ascorbic acid deficiency

  • scurvy
  • weakness
  • edema, gingivitis
  • bleeding gums
  • loss of teeth
  • anemia
  • subcu hemorrhage
  • bone lesions
  • delayed healing
141

Vitamin C action

required for collagen synthesis and maintenance of connective tissue, tissue repair, bone, teeth and capillary maintenance, folic acid metabolism, erythropoiesis, enhances absorption of iron, synthesis of lipids, proteins and steroids

142

Vitamin C source

citrus fruits and juices, tomatoes, strawberries, melons, spinach

143

Vitamin C adverse effects

megadoses result in n/v

HA, and cramping

acidifies urine--> may result in stones

144

Fat soluble vitamins

A,D,E,K