The Digestive System and
Ancillary Organs Part 1 of 2
1
Lecture Outline
I.
The Vomiting Reflex and Anti-Emetics
II.
GERD and Ulcers
III.
Diarrhea
IV.
The Defecation Reflex
V.
Constipation
VI.
Inflammatory Bowel Disease
VII. Bowel Infections
VIII. Diverticulitis
IX.
Colorectal Cancer
X.
The Gallbladder and its Disease States
XI.
The Liver and its Disease States
XII. Pancreatitis
2
Vomiting
3
Vomiting
• Vomiting is a complex reflex compared to the
knee jerk
• Multiple sensory inputs
• CNS processing component in the vomiting
center
• Motor component involves multiple motor
nerves and muscles
4
Introducing the Vomiting Reflex
Components of a Reflex
5
Introducing the Vomiting Reflex
Components of a Reflex
6
6
The Vomiting Reflex
7
The Vomiting Reflex
I. The motor
component of the
swallowing reflex
involves multiple
nerves and muscles.
II. Think of vomiting
as the approximate
reverse of swallowing
Kandel, et al., Principles of Neural Science, 3rd
ed., Elsevier, 1991, p.991.
8
8
Vomiting
Muscle Contraction
9
Vomiting
Muscle Contraction
• When you swallow, there is contraction of multiple
muscles
– Begin contracting muscles at the top of the throat and
then the contraction of the muscles moves down the
throat
– There is a big relaxation of the diaphragm so that the food
bolus can move down into the stomach
• The response must be coordinated
• Vomiting is backwards
– There is relaxation of the diaphragm and then contraction
of the muscles from the bottom up
10
The Vomiting Reflex
Diagram
11
Lehne, 2009, Pharmacolog
for Nursing
12 7th ed.,
12 Care,
Elsevier, p. 936
Vomiting
Sensory Components
13
Vomiting
Sensory Components
I. The sensory component of the vomiting reflex
involves multiple nerves and brainstem centers.
– Serotonin and dopamine sensors in the stomach
and small intestine go to the brain via the vagus
nerves
II. One part of the sensory component is actually in
the brain – the chemoreceptor trigger zone (CTZ).
– Sense noxious things in the blood
14
Vomiting
CNS Component
15
Vomiting
CNS Component
I. The CNS component is the vomiting center in
the medulla.
– Sensory input may come from sights,
smells, pain, higher centers (anticipation,
fear, memory), inner ear
16
Sensory Inputs to the Emetic
(Vomiting) Center
17
Sensory Inputs to the Emetic (Vomiting) Center
Emetic center in
the medulla,
a CNS
component
II. Chemoreceptor trigger
zone (CTZ), a
sensory
component
outside the
blood-brain
barrier
Hardman, et al, Goodman
& Gilman’s The
Pharmacologic Basis of
Therapeutics, 10th ed., 2001,
McGraw-Hill, p. 1030.
18
18
Sensory Inputs to the Emetic
(Vomiting) Center
19
Sensory Inputs to the Emetic
(Vomiting) Center
•
•
•
•
Higher centers
Inner ear---cerebellum
Pain, smell, and sight
Blood-borne emetics that are sensed in the
CTZ and then to the vomiting center
• Back of the throat
• Sensory nerves in the stomach and small
intestine
20
Vomiting
Receptor Areas
21
Vomiting
Receptor Areas
• Sensory information goes up the spinal cord to
the solitary tract nucleus (NTS)
• For motion sickness from the inner ear – H1
and muscarinic
• CTZ – serotonin, dopamine, muscarinic
• Stomach and small intestine – serotonin and
dopamine
• NTS – serotonin, dopamine, muscarinic, H1
22
Drugs that Interfere with Sensory
Input to the Vomiting Center
23
Drugs that Interfere with Sensory Input to the
Vomiting Center
1. Dopamine receptor antagonists affect the CTZ and the
Solitary Tract Nucleus (NTS) of the medulla.
2. Serotonin receptor antagonists (GI tract and NTS).
3. Muscarinic and histamine receptor antagonists (CTZ,
NTS, and inner ear).
4. Substance P Receptor antagonist (GI tract and brain).
5. Cannabanoids (?).
24
Dopamine Receptor Antagonists
25
Dopamine Receptor Antagonists
Many antipsychotic drugs have antiemetic properties. A few are
marketed as anti-emetics and are not used much as antipsychotics.
Dopamine antagonists used as anti-emetics
Generic Name
Trade name
Chlorpromazine
Thorazine
Perphenazine
Trilafon
Prochlorperazine
Compazine
Promethazine
Phenergan (Not for children <2 years old)
Metoclopramide (also blocks serotonin
receptors)
Reglan
Dromperidone
Motilium
26
Dopamine Receptor Antagonists
Function
27
Dopamine Receptor Antagonists
Function
• The oldest anti-nausea drugs
– Still are widely used
• They block dopamine receptors in the CTZ and the
nucleus of the solitary tract of the medulla.
• This prevents transmission of sensory information to
the vomiting center and lessens the likelihood of
vomiting.
– May or may not stop vomiting, depending on the
reason that the person is vomiting
28
Dopamine Receptor Antagonists
Adverse Effects
29
Dopamine Receptor Antagonists
Adverse Effects
• These drugs are also sedating, which may help
the nausea and vomiting.
• Adverse effects are the same as you learned
for the anti-psychotics, although tardive
dyskinesia is not as likely since the drugs are
not usually taken chronically for nausea.
30
Serotonin Receptor Antagonists
Introduction
31
Serotonin Receptor Antagonists
Introduction
•There are many subtypes of serotonin receptors, but the ones in the
stomach and CTZ are called 5-HT3 receptors (5-HT is an acronym for
serotonin, which is also called 5-hydroxytryptamine).
• Selective 5-HT3 receptor blockers have revolutionized the treatment
of chemotherapy-induced nausea.
• Unfortunately, these drugs are still relatively new and on patent
(ondonsetron just came off patent), so they are very expensive.
• Can be used together with the dopamine receptor antagonists.
•This leads to a pretty effective cocktail to stop vomiting
32
32
Serotonin Receptor Antagonists
Side Effects
33
Serotonin Receptor Antagonists
Side Effects
• Headache
• Diarrhea
• Dizziness
34
Serotonin Receptor Antagonists
Types of Drugs
35
5-HT3 Receptor Antagonists
Generic name
Brand name
Ondansetron
Zofran
Granisetron
Kytril
Dolasetron
Anzemet
Palonosetron
Aloxi
36
Muscarinic/Histamine Receptor
Antagonists
37
Muscarinic/Histamine Receptor Antagonists
• Muscarinic and/or H1 histamine receptors are involved
in the nausea of motion sickness.
• Many motion sickness pills have both antihistamine and
antimuscarinic activity.
• The scopolamine patch is antimuscarinic only.
38
Types of Muscarinic/Histamine
Receptor Antagonists
39
Antimuscarinic/Antihistaminic Antiemetics
Generic name
Brand name
Dimenhydrinate
Dramamine
AntiAntimuscarinic? histaminic?
Yes
Yes
Diphenhydramine
Benadryl
Yes
Yes
Hydroxyzine
Vistaril, Atarax
Yes
Yes
Meclizine
Bonine,
Antivert
Transderm
Scōp
Yes
Yes
Yes
No
Scopolamine
40
Substance P Receptor Antagonists
Also Known as NK1 Antagonists
Function
41
Substance P Receptor Antagonists
Also Known as NK1 Antagonists
Function
• Block the substance P receptors called NK1 that are
located on sensory nerves in the GI tract and in the brain.
• Aprepitant (Emend) is the only Substance P receptor
antagonist drug approved for nausea of chemotherapy.
Available as a prodrug (fosaprepitant) for IV use.
42
Substance P Receptor Antagonists
Adverse Effects
43
Substance P Receptor Antagonists
Adverse Effects
• It has substantial interactions with other drugs
at the level of the cytochrome P450 system,
including some chemo drugs, but apparently
not other antiemetics (See Lehne p. 939).
44
Cannabinoids
45
Cannabinoids
• Dronabinol (Marinol®) and nabilone (Cesamet®) are approved
for chemotherapy-associated nausea and vomiting.
• They activate cannabinoid receptors in the brain and periphery,
but it is not known how that relieves vomiting.
46
Cannabinoids
Adverse Effects
47
Cannabinoids
Adverse Effects
• They produce mental effects similar to
smoking marijuana but are not subject to
much abuse, possibly because of their slow
onset and high cost (and the ready availability
of marijuana). Dronabinol is Schedule III and
nabilone is Schedule II.
• These drugs can also cause tachycardia and
hypotension in susceptible patients.
48
Benzodiazepines
49
Benzodiazepines
• Lorazepam (Ativan) is commonly administered to
chemotherapy patients with their antiemetic.
• It is thought that the beneficial effect of lorazepam is
not really anti-emetic but amnesic.
• It prevents the chemo patient from remembering the
nausea and vomiting associated with chemotherapy
and thereby prevents anticipatory vomiting during the
next chemotherapy cycle.
• Before this strategy was adopted, patients would walk
into the chemotherapy facility and start vomiting.
50
Administration of Antiemetics
51
Administration of Antiemetics
• They could be administered p.o. ahead of anticipated
vomiting (before chemotherapy, for instance).
•In chemotherapy, they are usually given IV before
the treatment
• Some of them can be administered rectally.
•This is done rectally because if it is given orally, the
patient will vomit it back up
• Some of them can be administered IV or IM.
52
Which class of drugs is used both as
an anti-emetic and anti-psychotic?
53
Which class of drugs is used both as an anti-emetic
and anti-psychotic?
25% 25% 25% 25%
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1. Dopamine receptor
agonists
2. Cholinergic agonists
3. Serotonin antagonists
4. Dopamine receptor
antagonists
54
Gastroesophageal Reflux Disease
(GERD) and Ulcers
Diagram
55
Gastroesophageal Reflux Disease (GERD) and Ulcers
Diagram
McCance & Heuther, Pathophysiology, The Biologic Basis for Disease in Adults & Children, 2002, Mosby, p. 1267.
56
GERD
Description
57
GERD
Description
• The stomach is full of acid and the esophagus is not
• The lower esophageal sphincter is at the end of the
esophagus
– Sometimes it will allow the acidic contents of the stomach
to go into the esophagus
• Burns the esophagus, producing the symptom of heartburn
• In the diagram, the stomach protrudes up through the
diaphragm a little bit
– The protrusion of the stomach into the thoracic cavity is
called a hiatal hernia
• Increases the likelihood that there will be reflux
58
GERD
Signs and Symptoms
59
GERD
Signs and Symptoms
• GERD is extremely common, especially in individuals over 50
years old
•The presenting symptom is usually pain caused by the acid
contacting the esophagus.
• Initially, the damage is erosive esophagitis.
• After long-term reflux, the esophageal epithelium may change
from squamous to columnar, presumably as a defense mechanism.
• Later, a premalignant condition called Barrett’s esophagus may
develop.
• Esophageal cancer can develop from Barrett’s esophagus.
60
Control of GERD
61
Control of GERD
• Since the reflux is a normal phenomenon that may be exacerbated in some
people by structural abnormalities, it is hard to stop the reflux except by
altering the structure of the gastroesophageal junction through surgery.
•Reserved for the worse cases
•Over time, the structures stretch and the surgical repair will fail
•Consistently effective surgical procedures are under development.
•Enlisting the aid of gravity may help.
•Ask the person not to lie flat after eating (for two to three hours) and to
raise the head of the bed
•Get rid of the acid so that the reflux will not damage the esophagus.
•Drugs for GERD are the same as some of the anti-ulcer drugs, covered
below.
62
•One of the risks of GERD is aspiration
Cancer of the Esophagus
Diagram
63
Cancer of the Esophagus
Diagram
Esophageal cancer
Esophageal cancer
Barrett’s esophagus
Enzinger & Mayer, Esophageal Cancer, 2003, New Eng. J. Med.
349:2241-52.
64
Why Doesn’t the Stomach Digest Itself?
Diagram
65
Why Doesn’t the Stomach Digest Itself?
Diagram
66
Hardman and Limbird, Goodman & Gilman’s The Pharmacologic Basis of Therapeutics, 9th ed., McGraw-Hill, 1996, p.902.66
Why Doesn’t the Stomach Digest Itself?
Description
67
Why Doesn’t the Stomach Digest Itself?
Description
•
•
The secretions of the stomach prevent it from digesting itself
The final pathway of acid secretion is a molecule called the proton pump
– Requires energy in the form of ATP
– Exchanges a hydrogen ion for a potassium ion
•
Muscarinic receptors activate the pump
– M receptors are activated by the PNS, which is important in digestion
•
The presence of food in the stomach stimulates cells in the stomach to secrete
gastrin
– These also activate the proton pump
•
Histamine receptors (not H1, but H2) are activated by histamine and then activate
the proton pump
– The histamine comes from a nearby cell called the ECL cell
•
•
•
Prostaglandin receptors on the parietal cell bind to the receptors and inhibit the
proton pump
Activation of the proton pump causes acid secretion
Epithelial cells have prostaglandin receptor
– When stimulated by prost, they secrete mucus, as well as bicarbonate
•
The stomach does not digest itself because mucus and bicarbonate form a layer on
the surface of the stomach, which protects it from the acidic environment in the
stomach that is digesting the food
68
Mucosal Defenses Must be Greater
than Aggressive Factors to Prevent
the Formation of Ulcers
69
Mucosal Defenses Must be Greater than Aggressive
Factors to Prevent the Formation of Ulcers
Lehne, 2009,
Pharmacology
for Nursing Care,
7th ed., Elsevier,
p. 915
70
Causes of Peptic Ulcer Disease
71
Causes of Peptic Ulcer Disease
1.
Inadequate mucosal defenses (most common cause).
Helicobacter pylori infection.
- this is probably resonsible for 80-85% of stomach ulcers
Nonsteroidal anti-inflammatory therapy (NSAIDs also increase acid to some
extent).
- prost receptors promote mucus and bicarbonate secretion and inhibit acid
- NSAIDs inhibit the synthesis of prost so less mucus and bicarbonate is
secreted and there is less inhibition of the proton pump
- probably responsible for 10-15% of ulcers
2.
Too much acid (not the most common cause). Zollinger-Ellison syndrome.
72
Helicobacter pylori
Diagram
73
Helicobacter pylori
Diagram
74
Helicobacter pylori
A silver stain (Warthin Starry) of HP (black wiggly lines) on gastric mucus-secreting epithelial cells
(x1000). This picture is of Dr. Marshall's stomach biopsy, taken 8 days after he drank a culture of H.
pylori. This image is from the Helicobacter Foundation website: www.helico.com
75
Ulcer (and GERD) Treatment
Diagram
76
Ulcer (and GERD) Treatment
Diagram
Hardman and Limbird, Goodman & Gilman’s The Pharmacologic Basis of Therapeutics, 9th ed., McGrawHill, 1996, p.902.
77
Ulcer (and GERD) Treatment
Description
78
Ulcer (and GERD) Treatment
Description
• Give the person an antibiotic to get rid of the helicobacter
– Cure the ulcer and it will never come back
• Heal the ulcer
• Stop the stomach acid production
– Used chronically by people with GERD and acutely by people with an ulcer
• Drugs used
– Proton pump inhibitors
• Turn off all of the receptors
– Muscarinic antagonists
• Used to be used more but are not used as often now because of the negative side effects
– Histamine antagonists (H2)
• Ex. tagamet, zantac, pepsid
• The first type of drugs that are really good at stopping stomach acid
• 70-80% of stomach acid is due to H2 antagonists
79
Neutralize Acid
80
Neutralize Acid
Acid + base  salt and water
• Getting rid of acid is necessary for the ulcer to heal.
• Antacids neutralize acid that is already in the stomach.
• Antacids are bases that are consumed by the neutralization
reaction.
•If more acid is secreted, you have to take another dose of antacid.
•Antacids work very quickly: Maalox, Mylanta, Tums, etc.
•Work the quickest because they get rid of the acid that is already
present
•However, with someone who has a chronic problem, we want to
prevent acid secretion
81
Prevent Acid Secretion
82
Prevent Acid Secretion
• Acid secretion in the stomach is regulated by a number
of influences, per the diagram.
• However, the final step in acid secretion is secretion of
H+ into the lumen of the stomach by a large protein
called the proton pump.
• In preventing acid secretion, we have to decrease the
activity of the proton pump.
83
Ulcer (and GERD) Treatment
Diagram
84
Ulcer (and GERD) Treatment
Diagram
Lehne, 2009, Pharmacology for Nursing Care, 7th ed., Elsevier, p. 919
85
H2 Receptor Antagonists
86
H2 Receptor Antagonists
• Cimetidine (Tagamet®), ranitidine (Zantac®), famotidine (Pepcid®), and
nizatidine (Axid®).
• Since histamine receptors are responsible for a major portion of the
stimulation of the proton pump, blocking histamine receptors prevents
secretion of a major portion of the acid.
• These drugs do not prevent all acid secretion since there are other things that
simulate the proton pump.
• Cimetidine is of concern since it is an inhibitor of cytochrome P450 enzymes
and thereby can affect the metabolism of many drugs.
•Likes cimetidine the least
•Famotidine is probably the best one to take
•Famotidine complete is a combination of a pepcid and an antacid
87
Proton Pump Inhibitors
88
Proton Pump Inhibitors
•Drugs that block activity of the proton pump can be effective
in blocking all acid secretion.
•Omeprazole (Prilosec®), esomeprazole (Nexium®),
lansanoprazole (Prevacid®) and others.
•Most of these drugs are irreversible, that is, they bind
covalently to the proton pump and take it completely out of
action.
•The stomach cells can synthesize new proton pumps
•They can be taken once a day even though they have a short
half-life.
89
Proton Pump Inhibitors
Administration
90
Proton Pump Inhibitors
Administration
• They are destroyed by acid so they are enteric-coated or encased in little
granules that don’t dissolve until they reach the duodenum.
• If giving via N-G tube or gastrostomy, you can open the capsule and get the
granules out, but you shouldn’t crush the granules or the enteric coated
pill.
• After the pill or granules dissolve in the duodenum, the drug is absorbed
into the bloodstream and reaches the parietal cells of the stomach through the
bloodstream.
• Immediate-release powder with sodium bicarbonate (to neutralize stomach
acid) is available to be mixed with water for people with NG tubes or
gastrostomies
• IV preparations are available for esomeprazole, lansoprazole, and
pantoprazole.
91
Marketing of Esomeprazol
(Nexium)
92
Marketing of Esomeprazol (Nexium)
Stereoisomerism occurs at asymmetric carbons
Esomeprazole (Nexium) and omeprazole (Prilosec) are really the same drug –
esomeprazole is a pure stereoisomer and omeprazole is a racemic mixture
(the drug company has a new patent for esomeprazole and you need a
prescription, while omeprazole is over-the-counter – go figure!). Many
insurance company’s drug plans will pay for esomeprazole but not
omeprazole!
93
Treating H. pylori Infection
94
Treating H. pylori Infection
•Usually a combination of two or three antibiotics is
required.
•Treatment is usually for a full two weeks.
•Acid-suppressive therapy has to be included to heal the
ulcer.
•If the infection is eliminated, the ulcer will go away and
not return.
95
Which class of drugs provides the
FASTEST relief for GERD or the pain
of a peptic ulcer?
96
Which class of drugs provides the FASTEST relief for
GERD or the pain of a peptic ulcer?
25% 25% 25% 25%
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Antacids
Proton pump inhibitors
H2 receptor blockers
Anti-emetics
Pr
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1.
2.
3.
4.
97
Types of Diarrhea
98
Types of Diarrhea
1.
Osmotic
2.
Secretory – the cells in the intestines that normally secrete things into the
intestinal lumen, secrete huge quantities of fluids
3.
Shortened transit time caused by increased intestinal motility or bowelshortening surgery
4.
Loss of absorptive surface with secondary osmotic diarrhea (most viral
diarrheas and inflammatory bowel diseases)
- The villi and microvilli are very important in absorbing nutrients and
water into the bloodstream
- Many issues destroy the villi and microvilli so the contents cannot be
absorbed
5.
Many infectious diarrheas have two mechanisms–they cause loss of
absorptive surface and increased secretion
99
Mucosal Layers of the Intestine
100
Mucosal Layers of the Intestine
Cormack, DH, Essential Histology, 1993, Lippincott, plate 13.6.
101
Bacterial Causes of Severe (LifeThreatening) Diarrhea
102
Bacterial Causes of Severe (Life-Threatening) Diarrhea
1. Shigella.
2. Salmonellla
3. E. coli O157:H7
All 3 are of concern to public health officials
and might need to be reported.
103
Treatment of Diarrhea
104
Treatment of Diarrhea
• Many studies have shown that people get over
infectious diarrhea more quickly if the diarrhea is not
treated, except with rehydration.
•The best thing is just to remain hydrated and wait for
it to go away
• Rehydration with electrolyte solutions such as
Pedialyte, or in a pinch, Gatorade.
• Various pharmacologic agents have been used to stop
diarrhea, if necessary
105
Pharmacologic Treatment of
Diarrhea
106
Pharmacologic Treatment of Diarrhea
• Opioids are the most effective–any opioid would do, but the ones
that are used for diarrhea are taken orally and have low abuse
potential.
•The reason there is no abuse potential is that the drugs are poorly
absorbed, stay in the gut and do not cause systemic effects.
•Diphenoxylate HCL with atropine (Lomotil® and others) is a
combination of an opioid (diphenoxylate) and an antimuscarinic
drug (atropine).
• Atropine dries up secretions everywhere which can be problematic,
since the ones that we want to dry up are those in the bowel. Atropine
also slows GI motility.
107
Opioids
108
Opioids
• Loperamide (Imodium®) is an opioid that is poorly absorbed so it
has no systemic effects.
• Since the opioid drugs are administered to the intestine (by way of
the mouth and stomach), we could consider them topical drugs–they
bind to opioid receptors in the intestine to slow intestinal motility.
• There is very little evidence that kaolin preparations are effective
for diarrhea.
• There is no reason to use other opioids, such as paregoric, in
preference to diphenoxylate or loperamide.
109
Nervous System of the GI Tract
110
Nervous System of the GI Tract
Nervous control of the GI tract includes:
I. The enteric (myenteric) nervous system—an independent nervous
system that controls the GI tract independently of
influences from the spinal cord or brain.
- Keeps the food (and later stool) going in the correct
direction in a coordinating way
- There are as many or more neurons in the enteric nervous
system as in the brain
II. The sacral division of the parasympathetic nervous system
111
Myenteric Control of Defecation
112
Myenteric Control of Defecation
• Stretch of the rectum is communicated to the
myenteric nervous system via sensory nerves.
• The myenteric nervous system stimulates peristalsis
of the descending and sigmoid colon.
113
Rectal Sphincters
114
Rectal Sphincters
•The rectum has a smooth
muscle (internal) sphincter
that is under autonomic
control
•Skeletal muscle (external)
sphincter that is under
voluntary control.
Porth, 2007, Essential of Pathophysiology, 2nd ed., Lippincott, p. 596
115
Internal Smooth Muscle
Sphincter of the Rectum
116
Internal Smooth Muscle Sphincter of the Rectum
• The rectal smooth muscle sphincter is innervated by the autonomic nervous system.
• Normally, the smooth muscle sphincter is contracted.
• When the rectum is distended, sensory information is transmitted to
parasympathetic centers in the sacral cord.
• The parasympathetic center in the sacral cord processes the information and if the
sensory input is strong enough, sends motor impulses through parasympathetic
nerves leaving the sacrum supplying the smooth muscle sphincter, relaxing the
smooth muscle sphincter to permit defecation.
• This is accompanied by an urge to defecate.
•In infants, the urge to defecation results in defecation
•However, in non-babies, the external sphincter can help to control
defecation
117
External Skeletal Muscle
Sphincter of the Rectum
118
External Skeletal Muscle Sphincter of the Rectum
• The skeletal muscle sphincter is innervated by motor nerves.
• In toilet-trained individuals, the skeletal muscle sphincter can be
contracted to inhibit defecation until an appropriate time.
• When the person wishes to defecate, their cerebral cortex sends
impulses down the spinal cord and out through motor neurons in
spinal nerves to the skeletal muscle sphincter telling it to relax.
119
Defecation Reflex
Introduction
120
Defecation Reflex
Introduction
• If a person inhibits defecation too long, the parasympathetic
impulses will fatigue and the urge to defecate will disappear.
• At some later time, the parasympathetic defecation reflex will
again be activated, but each time it is inhibited and disappears, it
will be weaker when it returns.
• We can stimulate the defecation reflex by bearing down.
•That distends (stretches) the rectum and triggers the
defecation reflex.
121
The Defecation Reflex Pathway
122
The Defecation Reflex Pathway
The Defecation Reflex Pathway:
I. Sensory: Stretch receptors in the rectum communicate
with sacral parasympathetic centers.
II. CNS: Sacral parasympathetic centers evaluate the
sensory input and “decide” if defecation should occur.
III. Motor: Parasympathetic nerves carry impulses to the
rectum which relaxes the smooth muscle anal sphincter
(internal sphincter).
123
Defecation Reflex Pathway
Diagram
124
125
125
Which of the following is/are under
voluntary control and is/are
responsible for limiting defecation to
appropriate times/places in toilettrained individuals?
126
Which of the following is/are under voluntary control and
is/are responsible for limiting defecation to appropriate
times/places in toilet-trained individuals?
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1.
...
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127
Constipation
128
Constipation
• Constipation is difficult defecation, such as feeling like you need to
go but not being able to—not lack of a bowel movement on a given
day.
129
Constipation
Treatment
130
Constipation
Treatment
1. Dietary modification
- Increase intake of fiber
2. Going to the toilet when the defecation reflex is
the strongest (when it first appears).
3. Laxatives or enemas (except fiber agents or stool
softeners) should never be used for day-to-day
bowel control.
131
Laxatives
132
Laxatives
1. Bulk-forming agents (fiber).
2. Surfactant laxatives (stool softeners).
3. Osmotic laxatives.
4. Stimulant laxatives.
- According to McLeskey, this is the only
category of true laxatives
- Try to avoid these unless necessary
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Bulk-forming Agents
134
Bulk-forming Agents
• Classified as laxatives, but they really just soften the stool by
increasing its mass and holding in water.
•A nicer name for these agents is “fiber.”
• Ex.: Methylcellulose, psyllium (Metamucil) and polycarbophil.
• These drugs are used to supplement the fiber normally found in the
diet, which Americans don’t eat enough of.
• Effects might not be noted for 1-3 days.
135
Bulk-Forming Agents
Adverse Effects
136
Bulk-Forming Agents
Adverse Effects
• Can cause cramping, flatulence and mild
diarrhea in larger quantities or when added to
the person’s diet suddenly.
• If added slowly and increased gradually, these
effects are not prominent.
137
Surfactant Laxatives (Stool
Softeners)
138
Surfactant Laxatives (Stool Softeners)
• Docusate (Colace and others).
• Retain water in the stool and increase the
secretion of water in the large bowel.
• Can cause diarrhea in large quantities but
usually don’t.
139
Osmotic Laxatives
140
Osmotic Laxatives
• Hold water in the stool
•Do this slightly better than the stool softeners
• Salts of magnesium (Milk of Magnesia (magnesium
hydroxide) or magnesium citrate), polyethylene glycol
(MiraLax, with or without electrolytes), lactulose.
• If given in large quantities can cause diarrhea, but
smaller quantities produce semi-fluid stool.
• Polyethylene glycol preparations are used for
constipation (MiraLax) and to cleanse the bowel before
colonoscopy or other procedures.
141
Stimulant Laxatives
142
Stimulant Laxatives
• Bisacodyl (Ducolax, Correctol), senna, castor oil.
• Stimulate peristalsis and increase the secretion of water.
• Castor oil works in the small intestine as well as the colon,
so it is the most effective.
• These laxatives will produce a semisolid stool or a watery
stool.
•These are the laxatives that are sometimes abused so that
people become dependent on them to have a bowel
movement.
143
Inflammatory Bowel Disease
144
Inflammatory Bowel Disease
• Perhaps autoimmune in nature.
• Crohn’s disease affects the large and small bowel,
sometimes in a patchy pattern (a.k.a. regional enteritis)
•Can affect areas of the GI tract above the intestine
•Ulcerative colitis affects only the large bowel.
145
Inflammatory Bowel Disease
Signs and Symptoms
146
Inflammatory Bowel Disease
Signs and Symptoms
• The both cases, inflammation destroys the epithelium and the
absorptive surface of the intestine and causes bleeding, which
can be serious.
• Both are associated with anemia due to chronic blood loss.
• Bloody diarrhea is the prominent symptom.
• Both are associated with an increased risk of colon cancer.
• Both are associated with malabsorption due to loss of
absorptive surface and sometimes due to surgery that
removed affected parts of the intestine
147
Inflammatory Bowel Diseases
Treatment
148
Inflammatory Bowel Diseases
Treatment
• Pharmacologic treatment is immunosuppressive.
•Some of the same drugs that are used in organ transplantation
are used in inflammatory bowel diseases.
• Steroids are also used for their anti-inflammatory and
immunosuppressive properties.
• Side effects of these treatments are covered elsewhere in this
course.
• Surgery to remove portions of the bowel that are destroyed by
chronic inflammation may be necessary.
149