Week 4b Gastrointestinal Pathophysiology Flashcards
1
Q
What is an ileus?
A
A transient cessation of coordinated bowel motility after surgical intervention,
which prevents effective transit of intestinal contents and/or tolerance of oral
intake
2
Q
What are 4 factors that can contribute to an ileus?
A
- Manipulation of the bowel -main factor
- Electrolyte imbalances
- Fluid shifts (too much fluid = swelling of the gut = ↑ ileus)
- Intestinal wall swelling
3
Q
How long can an ileus last after surgery?
A
3-4 days
4
Q
How does surgical manipulation lead to an ileus?
A
Surgical manipulation increases sympathetic stimulation of the myenteric plexus, which promotes the influx of leukocytes into the “traumatized” areas of the gut and creates inflammatory cascade
5
Q
What can an untreated ileus lead to and why?
A
peritonitis, if leaked bacteria cannot be phagocytosed by the body
6
Q
What can help attenuate ileus incidence?
A
regional anesthesia
7
Q
What are the 6 causes of mesenteric ischemia?
A
- strangulation
- emboli
- aortic X-clamping
- trauma
- atherosclerosis
- inflammation
8
Q
What are the three treatment steps for mesenteric ischemia?
A
- reperfusion
- revascularization
- bowel resection
9
Q
What is the primary function of the colon?
A
water absorption
10
Q
Is full colonic resection compatible with life?
A
yes
11
Q
What is the primary function of the jejunum?
A
primary site for digestion & absorption of nutrients
12
Q
Is jejunal resection compatible with life?
A
yes, usually the ileum is able to adapt
13
Q
What is the primary function of the ileum?
A
absorption of B12 & bile salts
14
Q
What happens with resection of the ileum?
A
bile will enter the colon & stimulate fat and water secretion
15
Q
Why is motor activity disrupted after a bowel anastomosis?
A
transection of the pacemaker myogenic cells
16
Q
What part of the anastomosis has disruption in the motor activity?
A
the distal part of the anastomosis…
must rely on its own intrinsic slow-wave transmission
17
Q
What nerves innervate the parietal peritoneum, abdominal wall muscles, and skin?
A
the ventral rami of thoracoabdominal nerves
18
Q
The ventral rami of the thoracoabdominal nerves innervate:
A
parietal peritoneum, abdominal wall muscles, and skin
19
Q
Spinal cord segments T5-L2 innervate __ of the GI tract:
A
upper abdomen:
- liver
- stomach
- pancreas
- small bowel
- proximal part of the colon
20
Q
Spinal cord segments T9-L3 innervate ___ of the GI tract:
A
lower abdomen:
- descending colon
- sigmoid & rectum
- bladder
- lower ureter
21
Q
Fibers from spinal cord segments S2-S4 innervate:
A
colon, rectum, internal and external genitalia & bladder
22
Q
Sympathetic afferent fibers transmit:
A
visceral pain
23
Q
Sympathetic efferent nerves:
A
- inhibit peristalsis
- gastric distention
- GI vasoconstriction
24
Q
In the GI tract, the parasympathetic nervous system supplies the abdominal viscera via ___-
A
the vagus nerve
25
Afferent parasympathetic nerve fibers control:
sensations of satiety, nausea, & distention
26
Efferent parasympathetic nerve fibers increase:
functions of secretion, sphincter relaxation, peristalsis
27
How is abdominal visceral pain different from somatic pain?
1. poorly controlled
2. strong affective responses
3. refers to other locations
4. emotional association
28
What is the treatment for abdominal visceral pain?
- opioids
- NSAIDS
- acetaminophen
- regional anesthesia
29
In the treatment of abdominal visceral pain, regional anesthesia techniques that can be used:
1. spinal
2. epidural
3. paravertebral
4. selective nerve plexus blocks
30
Regional anesthesia often blocks ____ but not ____
sympathetic, but not parasympathetic
31
Why might regional anesthesia fail in treating abdominal visceral pain?
failure may occur due to multiple cross plexus innervations
32
When combining with another major regional technique, what kind of local anesthetics are required to treat abdominal visceral pain?
dilute local anesthetics
33
What are 4 congenital anomalies of the GI tract?
1. Atresia/fistulas
2. Meckel diverticulum
3. Hirschsprung disease
4. Malrotation & midgut volvulus
34
What is the presenting symptom of atresias and fistulas?
inability to feed & regurgitation shortly after birth
35
What is the presenting symptom of atresias and fistulas?
| 5
inability to feed & regurgitation shortly after birth
- excessive secretions
- coughing
- choking after first feeding
- recurrent pneumonias
- OG cannot be passed
36
What is the survival of infants with TEF and no other congenital anomalies?
>95%
37
What is the survival of infants with TEF and no other congenital anomalies?
>95%
38
What are the risks of tracheoesophageal fistula (TEF) & esophageal atresia (EA)?
(3)
1. pneumonia
2. poor nutrition
3. gastric distention that may impair respiration
39
How/when are tracheoesophageal fistula (TEF) & esophageal atresia (EA) normally diagnosed?
immediately after birth when a newborn has
1. excessive secretions
2. coughing
3. choking after first feeding
40
How many types of tracheoesophageal fistula (TEF) & esophageal atresia (EA) are there?
5
41
Treatment of tracheoesophageal fistula (TEF) & esophageal atresia (EA) include?
surgical repair; ligation of fistula & anastomosis of esophagus
42
What are the 5 types of tracheoesophageal fistula (TEF) &/or esophageal atresia (EA)?
1. esophageal atresia with distal tracheoesophageal fistula
2. isolated esophageal atresia
3. isolated tracheoesophageal fistula
4. esophageal atresia with proximal tracheoesophageal fistula
5. esophageal atresia with double tracheoesophageal fistula
43
What is a diverticulum?
blind outpouching of the alimentary track;
includes all 3 layers of the bowel wall
- can mimic appendicitis
- painless rectal bleeding in toddlers
44
What is a "classic" sign of meckel diverticulum?
painless rectal bleeding in toddlers
45
What can meckel diverticulum mimic?
appedicitis
46
Where does meckel diverticulum occur?
in the ileum
47
What is the cause of meckel diverticulum?
mal-formation & remnant of the omphalomesenteric duct.
→ normally the omphalomesenteric duct connects the embryonic midgut to the yolk sac
[this provides nutrients to the midgut during embryonic development]
normally this duct narrows & disappears between 5th and 8th weeks gestation
48
What abnormality is associated with the "rule of 2s"?
meckel diverticulum
49
What is the rule of 2s?
* Occurs in 2% of the population
* 2-inches in length and within 2 feet of ileocecal valve
* Symptomatic by age 2 and twice as common in males
50
What is Hirschsprung disease?
congenital disorder that causes intestinal obstruction from birth
defective innervation of the colon due to the failure of migration of neural crest cells
lack the ganglion cells of the Meissner & Auerbach enteric neural plexuses
51
What is the cause of s/s in Hirschsprung disease?
lack of the ganglion cells of the Meissner & Auerbach enteric neural plexuses
→ lack of peristaltic contractions in the distal colon; creating a functional block
52
What is always affected in Hirschsprung disease?
the rectum
53
What is the treatment/surgical intervention for Hirschsprung disease?
- Pull through surgery or resection to bypass and remove the part of the colon
that lacks nerve cells
- Ostomy
- Rectal irrigations
- disimpaction
54
How is a definitive diagnosis of Hirschsprung disease made?
ganglion cells are absent in rectal biopsy
55
What causes malrotation & midgut volvlus?
abnormal migration or incomplete rotation of the intestines from the yolk sac back into the abdomen
56
What is the pathophysiology of malrotation & midgut volvulus?
* Intestines twisted around the superior mesenteric artery may produce kinking or compression of the vascular supply
* May result in atretic segments, compromised perfusion, and intestinal ischemia
57
What is "volvulus"?
bowel strangulation & shock
58
How do malrotation/volvulus cases present?
1/3 within the first week of life with:
- bilious vomiting
- distended abdomen
- hemodynamic instability
- hypotension
- hypovolemia
- electrolyte abnormalities
- bloody stools are an ominous sign
59
What is an ominous sign of malrotation/volvulus?
bloody stools
60
When is surgery for malrotation/volvulus?
immediately, it is an emergency!
[d/t risk of necrosis]
61
How does surgery treat volvulus?
reduces the volvulus & relieves the obstruction by dividing the fixation bands between the cecum and the duodenum or jejunum & widens the base of the mesentery.
62
When do children develop short gut?
with less than 30-40cm of small bowel
[need TPN}
63
What kind of vomiting is seen in malrotation with volvulus?
bilious
| rarely nonbilious vomiting
64
What is Ladd's procedure for?
alleviate intestinal malrotation
65
What is involved in a Ladd's procedure? (5)
Involves:
1. counterclockwise detorsion of the bowel
2. surgical division of Ladd's
bands
3. widening of the small intestine's mesentery
4. performing an
appendectomy
5. reorientation of the
small bowel on the right and the cecum and colon on the left
66
What are the 4 pathophysiologies of the esophagus?
1. esophageal obstruction
2. achalasia
3. varices
4. esophagitis
a. chronic acid reflux
b. barrett esophagus
c. eosinophilic esophagitis
67
What are the 3 kinds of esophagitis?
a. chronic acid reflux
b. barrett esophagus
c. eosinophilic esophagitis
68
What are the 2 categories (& 2 in each category) of esophageal obstruction?
1. Mechanical obstruction
- foreign body aspiration
- tumors
a. adenocarcinoma
b. squamous cell carcinoma
2. Functional (aka Achalasia; damaged nerves in the esophagus)
a. defects in LES tone
b. inflammatory degermation of neurons in the distal esophagus
69
What are 2 types of esophageal tumor?
a. adenocarcinoma
| b. squamous cell carcinoma
70
What are 3 possible defects in LES tone?
- incomplete relaxation
- increased tone
- esophageal aperistalsis
71
What is Achalasia?
neuromuscular disorder of the esophagus; in ability of the LES to relax, leading to a dilated esophagus
72
What is the pathophysiology of achalasia?
loss of ganglion cells in the myenteric plexus due to a degenerative neuronal disease or infection
73
What are the symptoms of achalasia?
- dysphagia
- regurgitation
- heartburn
- chest pain
74
What is the cause of esophageal varices?
portal hypertension
75
What are esophageal varices?
development of collateral channels to shunt blood from the portal circulation to the caval circulation, creating dilated veins (varices)
76
Where do esophageal varices occur?
in the distal esophagus & proximal stomach
77
What is the mortality of patients with esophageal varices?
High mortality:
- Cirrhotic patients 40-70%
- non cirrhotic 5-10%
30% of initial bleeding episodes are fatal
78
What % of initial bleeding (esophageal varices) episodes are fatal?
30%
79
What is the treatment for variceal bleeding?
1. Pharmacologic treatments
2. Sclerosant Injection
3. Banding
4. Balloon tamponade
5. TIPS - trans-jugular intrahepatic portosystemic shunt
6. Surgical shunt
80
What is a Blakemore tube?
NG tube with 2 balloons;
1 esophageal
1 gastric
tension should be held on it with 250-500g
81
What else do you need if the patient has a Blakemore tube?
secure airway*
82
What is the time limit for a Blakemore Tube?
should not be in place >6 hours
83
What is a mesocaval shunt?
A portosystemic shunt between the superior mesenteric vein and the inferior vena cava to reduce portal hypertension
84
What is esophagitis?
Inflammation of the lining of the esophagus may be caused by gastric acid, ingested chemicals, immune reactions, and infectious agents
85
What are causes of esophagitis?
- gastric acid
- ingested chemicals
- immune reactions
- infectious agents
86
What is reflux esophagitis?
Esophageal mucosa exposed to gastric acid over time will develop
inflammation and injury
87
What are causes of reflux esophagitis?
Decreased LES or increased abdominal pressure
- alcohol and tobacco use
- obesity
- central nervous system depressants
- pregnancy
- hiatal hernia
- delayed gastric emptying
- increased gastric volume
88
What is the pathophysiology of reflux esophagitis?
- Irritation leads to mucosa inflammation
- Infiltrated with eosinophils and neutrophils
- Can lead to ulcerations, infections, and perforation
89
What are symptoms of reflux esophagitis?
- heartburn
- dysphagia
- regurgitation of sour gastric contents
- Chest pain which can be mistaken for heart disease
90
What is Barrett esophagus?
complication of chronic GERD
- Metaplastic conversion of normal squamous esophageal epithelium to columnar epithelium
→ may involve a genetic predisposition (TP53 mutations)
91
Barrett esophagus is a precursor to ___.
adenocarcinoma
92
When is Barrett esophagus diagnosed?
often at advanced stages
93
What is eosinophilic esophagitis?
- inflammatory condition in response to allergens in food (milk, soy)
94
What is eosinophilic esophagitis associated with?
other forms of atopy
→ atopic dermatitis
→ allergic rhinitis
→ asthma
95
What is the pathophysiology of eosinophilic esophagitis?
Eosinophils are present in the esophageal mucosa, typically in far greater
numbers than in GERD
→ May also include upper and mid esophagus
96
Symptoms of eosinophilic esophagitis:
- dysphagia
| - intolerance of foods with the allergen
97
What is the treatment for eosinophilic esophagitis?
- PPIs are of limited efficacy
- exclusion of offending allergen
- systemic steroids
98
What are 3 stomach pathophysiologies?
1. gastritis [acute, chemical, stress-related, H.pylori]
2. peptic ulcer disease
3. neuroendocrine tumors
99
What is gastritis?
inflammation of the gastric mucosa
100
What is the cause of gastritis?
* Exposure to acid and other injurious agents
| * An imbalance between damaging factors and mechanisms that protect the stomach lining from these agents
101
What are symptoms of acute gastritis?
* May be asymptomatic
* Epigastric pain, nausea, and vomiting
* Ulceration and hemorrhage, resulting in hematemesis (vomiting of blood)
102
What is the pathology of acute gastritis?
* Stomach is normally strongly acidic (pH close to 1)
* Contains proteases and other enzymes that can be damaging
• Usually is shield from damage by
→ Mucin – thin layer of mucus in the mucosa secreted by surface epithelial cells that has a neutral pH (secretes bicarb)
→ Blood supply – efficiently buffers and removes caustic agents
• Injuries – NSAIDS, H. pylori, chemicals
103
In acute gastritis, where are neutrophils?
within the epithelial layer
104
What are common causes of chemical gastritis?
- NSAIDs
- Uremia & infection by H. pylori
- Chemical exposures
105
How do NSAIDs cause chemical gastritis?
Inhibit production of prostaglandins, which normally stimulate mucin and bicarbonate secretion and mucosal blood flow
106
How does uremia & infection by H.pylori cause chemical gastritis?
may inhibit gastric bicarbonate transporters
107
How do chemical exposures cause chemical gastritis?
Acids and alkalis, alcohol, and chemotherapeutic drugs, may directly injure the gastric mucosa
108
Who is prone to developing stress-related gastritis?
patients with:
- severe trauma
- burns
- extensive surgery
- critical illness
109
Pathology of stress-related gastritis:
* Local ischemia due to systemic hypotension or reduced blood flow caused by SNS-induced vasoconstriction
* Increased acid production secondary to stimulation
* Systemic acidosis may exacerbate the damage by lowering the intracellular pH of mucosal cells
* Does not usually result in scarring like in peptic ulcer disease
110
What is H.pylori?
a spiral-shaped bacillus detectable in gastric mucosal biopsies from many patients with duodenal ulcer and chronic gastritis
111
H. pylori gastritis is common in:
- children
- crowded living conditions
- poor sanitation
112
H. pylori infection is associated with:
an increased risk of gastric carcinoma
113
Pathology of H.pylori:
* Bacterial enzymes and other toxic products that directly damage epithelial cells
* Increased production of gastric acid, in part by stimulating gastrin secretion and in part by reducing the production of physiologic inhibitors of acid secretion
* Production of proteases that degrade normally protective glycoproteins in the mucous layer, exposing epithelial cells to the harsh gastric contents
* Stimulation of acute and chronic inflammation and cytokine release
114
What are symptoms of H.pylori gastritis:
typical signs of gastritis (pain, N/V)
115
How is H.pylori gastritis diagnosis:
* Gastric biopsies to identify immunohistochemical stains and cultures
* Breath tests - ureases produced by the bacteria break down urea into ammonia
* Stool test - presence of H. pylori antigen
116
What is peptic ulcer disease?
A benign ulcer composed of granulation tissue and necrotic cell debris and inflammatory cells resting on a fibrous scar
117
peptic ulcer disease results from:
excess gastric acid and an impaired mucosal defense
often the consequence of H. pylori infection and chronic NSAID use
118
What anatomical location & age range is peptic ulcer disease most common:
More frequent in the duodenum than in the stomach and seen in
middle-age or older adults
119
What is the treatment for gastritis?
- antacids
- H2 receptor antagonists
- proton pump inhibitors
- prostaglandin analogues
120
Antacids as treatment for gastritis:
- aluminum hydroxide
- magnesium hydroxide (e.g., Maalox, Mylanta)
- calcium carbonate (Tums)
• symptomatic relief of dyspepsia
121
H2 receptor antagonists for treatment of gastritis:
- cimetidine
- ranitidine
- famotidine
- nizatidine
• inhibit basal and stimulated gastric acid secretion
122
Proton pump inhibitors for treatment of gastritis:
- omeprazole
- esomeprazole
- lansoprazole
- rabeprazole
- pantoprazole
• covalently bind and irreversibly inhibit hydrogen potassium–adenosine triphosphatase (H + ,K + -ATPase)
123
Prostaglandin analogues for treatment of gastritis:
- misoprostol
• enhance mucosal bicarbonate secretion, stimulate mucosal blood flow, and decrease mucosal cell turnover
124
Polyps:
inflammatory abnormal tissue when cells grow and divide more they should or do not die when they should
• frequent incidental findings in endoscopies
125
When are polyps usually found:
frequently an incidental findings in endoscopies
126
Adenoma:
abnormal tissue that may serve as precursors for cancers
127
What type of epithelia dysplasia is found in adenomas?
varying degrees
128
What is the most common malignancy of the stomach?
adenomas;
- idiopathic
- familial adenomatous polyposis syndrome
- H.pylori - induced
- Epstein-Barr virus (EBV) infection
129
Do adenomas spread or stay localized?
can spread locally to involve the duodenum, pancreas & retroperitoneum
130
Where do adenomas spread?
locally to duodenum, pancreas, & retroperitoneum
131
What is a neuroendocrine tumor?
a type of tumor that grows from neuroendocrine cells
132
What do neuroendocrine cells do?
send and receive messages through hormones to help the body function
133
Where are neuroendocrine cells found?
in all organs throughout the body
134
Do carcinoid tumors grow slow or fast?
slow
135
Where are most carcinoid tumors found?
75% are found in the GI tract (often in the small intestine)
25% are found in the lungs
136
What type of neuroendocrine tumors rarely spread?
foregut neuroendocrine tumors
[stomach, duodenum, esophagus]
137
Where are foregut neuroendocrine tumors?
- stomach
- duodenum
- esophagus
138
What type of tumor increases gastric acid production, causing ulcers?
gastrinomas
139
What is the cause of Zollinger-Ellison syndrome?
gastrinomas that increase gastric acid production, leading to ulcers
140
Where are midgut carcinoid tumors?
small intestine
141
What are characteristics of midgut carcinoid tumors?
located in the small intestine, often multiple and aggressive
142
Where are hindgut carcinoid tumors located?
appendix and colon
143
What are characteristics of hindgut tumors?
usually incidental and benign
