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N935 Advanced Pathophysiology > Week 4b Gastrointestinal Pathophysiology > Flashcards

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

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2
Q

What are 4 factors that can contribute to an ileus?

A
  1. Manipulation of the bowel -main factor
  2. Electrolyte imbalances
  3. Fluid shifts (too much fluid = swelling of the gut = ↑ ileus)
  4. Intestinal wall swelling
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3
Q

How long can an ileus last after surgery?

A

3-4 days

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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

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5
Q

What can an untreated ileus lead to and why?

A

peritonitis, if leaked bacteria cannot be phagocytosed by the body

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6
Q

What can help attenuate ileus incidence?

A

regional anesthesia

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7
Q

What are the 6 causes of mesenteric ischemia?

A
  1. strangulation
  2. emboli
  3. aortic X-clamping
  4. trauma
  5. atherosclerosis
  6. inflammation
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8
Q

What are the three treatment steps for mesenteric ischemia?

A
  1. reperfusion
  2. revascularization
  3. bowel resection
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9
Q

What is the primary function of the colon?

A

water absorption

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10
Q

Is full colonic resection compatible with life?

A

yes

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11
Q

What is the primary function of the jejunum?

A

primary site for digestion & absorption of nutrients

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12
Q

Is jejunal resection compatible with life?

A

yes, usually the ileum is able to adapt

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13
Q

What is the primary function of the ileum?

A

absorption of B12 & bile salts

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14
Q

What happens with resection of the ileum?

A

bile will enter the colon & stimulate fat and water secretion

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15
Q

Why is motor activity disrupted after a bowel anastomosis?

A

transection of the pacemaker myogenic cells

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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

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17
Q

What nerves innervate the parietal peritoneum, abdominal wall muscles, and skin?

A

the ventral rami of thoracoabdominal nerves

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18
Q

The ventral rami of the thoracoabdominal nerves innervate:

A

parietal peritoneum, abdominal wall muscles, and skin

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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
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20
Q

Spinal cord segments T9-L3 innervate ___ of the GI tract:

A

lower abdomen:

  • descending colon
  • sigmoid & rectum
  • bladder
  • lower ureter
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21
Q

Fibers from spinal cord segments S2-S4 innervate:

A

colon, rectum, internal and external genitalia & bladder

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22
Q

Sympathetic afferent fibers transmit:

A

visceral pain

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23
Q

Sympathetic efferent nerves:

A
  • inhibit peristalsis
  • gastric distention
  • GI vasoconstriction
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24
Q

In the GI tract, the parasympathetic nervous system supplies the abdominal viscera via ___-

A

the vagus nerve

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25
Q

Afferent parasympathetic nerve fibers control:

A

sensations of satiety, nausea, & distention

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26
Q

Efferent parasympathetic nerve fibers increase:

A

functions of secretion, sphincter relaxation, peristalsis

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27
Q

How is abdominal visceral pain different from somatic pain?

A
  1. poorly controlled
  2. strong affective responses
  3. refers to other locations
  4. emotional association
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28
Q

What is the treatment for abdominal visceral pain?

A
  • opioids
  • NSAIDS
  • acetaminophen
  • regional anesthesia
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29
Q

In the treatment of abdominal visceral pain, regional anesthesia techniques that can be used:

A
  1. spinal
  2. epidural
  3. paravertebral
  4. selective nerve plexus blocks
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30
Q

Regional anesthesia often blocks ____ but not ____

A

sympathetic, but not parasympathetic

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31
Q

Why might regional anesthesia fail in treating abdominal visceral pain?

A

failure may occur due to multiple cross plexus innervations

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32
Q

When combining with another major regional technique, what kind of local anesthetics are required to treat abdominal visceral pain?

A

dilute local anesthetics

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33
Q

What are 4 congenital anomalies of the GI tract?

A
  1. Atresia/fistulas
  2. Meckel diverticulum
  3. Hirschsprung disease
  4. Malrotation & midgut volvulus
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34
Q

What is the presenting symptom of atresias and fistulas?

A

inability to feed & regurgitation shortly after birth

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35
Q

What is the presenting symptom of atresias and fistulas?

5

A

inability to feed & regurgitation shortly after birth

  • excessive secretions
  • coughing
  • choking after first feeding
  • recurrent pneumonias
  • OG cannot be passed
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36
Q

What is the survival of infants with TEF and no other congenital anomalies?

A

> 95%

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37
Q

What is the survival of infants with TEF and no other congenital anomalies?

A

> 95%

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38
Q

What are the risks of tracheoesophageal fistula (TEF) & esophageal atresia (EA)?
(3)

A
  1. pneumonia
  2. poor nutrition
  3. gastric distention that may impair respiration
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39
Q

How/when are tracheoesophageal fistula (TEF) & esophageal atresia (EA) normally diagnosed?

A

immediately after birth when a newborn has

  1. excessive secretions
  2. coughing
  3. choking after first feeding
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40
Q

How many types of tracheoesophageal fistula (TEF) & esophageal atresia (EA) are there?

A

5

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41
Q

Treatment of tracheoesophageal fistula (TEF) & esophageal atresia (EA) include?

A

surgical repair; ligation of fistula & anastomosis of esophagus

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42
Q

What are the 5 types of tracheoesophageal fistula (TEF) &/or esophageal atresia (EA)?

A
  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
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43
Q

What is a diverticulum?

A

blind outpouching of the alimentary track;

includes all 3 layers of the bowel wall

  • can mimic appendicitis
  • painless rectal bleeding in toddlers
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44
Q

What is a “classic” sign of meckel diverticulum?

A

painless rectal bleeding in toddlers

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45
Q

What can meckel diverticulum mimic?

A

appedicitis

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46
Q

Where does meckel diverticulum occur?

A

in the ileum

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47
Q

What is the cause of meckel diverticulum?

A

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

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48
Q

What abnormality is associated with the “rule of 2s”?

A

meckel diverticulum

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49
Q

What is the rule of 2s?

A
  • 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
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50
Q

What is Hirschsprung disease?

A

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

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51
Q

What is the cause of s/s in Hirschsprung disease?

A

lack of the ganglion cells of the Meissner & Auerbach enteric neural plexuses

→ lack of peristaltic contractions in the distal colon; creating a functional block

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52
Q

What is always affected in Hirschsprung disease?

A

the rectum

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53
Q

What is the treatment/surgical intervention for Hirschsprung disease?

A
  • Pull through surgery or resection to bypass and remove the part of the colon
    that lacks nerve cells
  • Ostomy
  • Rectal irrigations
  • disimpaction
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54
Q

How is a definitive diagnosis of Hirschsprung disease made?

A

ganglion cells are absent in rectal biopsy

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55
Q

What causes malrotation & midgut volvlus?

A

abnormal migration or incomplete rotation of the intestines from the yolk sac back into the abdomen

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56
Q

What is the pathophysiology of malrotation & midgut volvulus?

A
  • 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
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57
Q

What is “volvulus”?

A

bowel strangulation & shock

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58
Q

How do malrotation/volvulus cases present?

A

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
Q

What is an ominous sign of malrotation/volvulus?

A

bloody stools

60
Q

When is surgery for malrotation/volvulus?

A

immediately, it is an emergency!

[d/t risk of necrosis]

61
Q

How does surgery treat volvulus?

A

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
Q

When do children develop short gut?

A

with less than 30-40cm of small bowel

[need TPN}

63
Q

What kind of vomiting is seen in malrotation with volvulus?

A

bilious

rarely nonbilious vomiting

64
Q

What is Ladd’s procedure for?

A

alleviate intestinal malrotation

65
Q

What is involved in a Ladd’s procedure? (5)

A

Involves:
1. counterclockwise detorsion of the bowel

  1. surgical division of Ladd’s
    bands
  2. widening of the small intestine’s mesentery
  3. performing an
    appendectomy
  4. reorientation of the
    small bowel on the right and the cecum and colon on the left
66
Q

What are the 4 pathophysiologies of the esophagus?

A
  1. esophageal obstruction
  2. achalasia
  3. varices
  4. esophagitis
    a. chronic acid reflux
    b. barrett esophagus
    c. eosinophilic esophagitis
67
Q

What are the 3 kinds of esophagitis?

A

a. chronic acid reflux
b. barrett esophagus
c. eosinophilic esophagitis

68
Q

What are the 2 categories (& 2 in each category) of esophageal obstruction?

A
  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
Q

What are 2 types of esophageal tumor?

A

a. adenocarcinoma

b. squamous cell carcinoma

70
Q

What are 3 possible defects in LES tone?

A
  • incomplete relaxation
  • increased tone
  • esophageal aperistalsis
71
Q

What is Achalasia?

A

neuromuscular disorder of the esophagus; in ability of the LES to relax, leading to a dilated esophagus

72
Q

What is the pathophysiology of achalasia?

A

loss of ganglion cells in the myenteric plexus due to a degenerative neuronal disease or infection

73
Q

What are the symptoms of achalasia?

A
  • dysphagia
  • regurgitation
  • heartburn
  • chest pain
74
Q

What is the cause of esophageal varices?

A

portal hypertension

75
Q

What are esophageal varices?

A

development of collateral channels to shunt blood from the portal circulation to the caval circulation, creating dilated veins (varices)

76
Q

Where do esophageal varices occur?

A

in the distal esophagus & proximal stomach

77
Q

What is the mortality of patients with esophageal varices?

A

High mortality:

  • Cirrhotic patients 40-70%
  • non cirrhotic 5-10%

30% of initial bleeding episodes are fatal

78
Q

What % of initial bleeding (esophageal varices) episodes are fatal?

A

30%

79
Q

What is the treatment for variceal bleeding?

A
  1. Pharmacologic treatments
  2. Sclerosant Injection
  3. Banding
  4. Balloon tamponade
  5. TIPS - trans-jugular intrahepatic portosystemic shunt
  6. Surgical shunt
80
Q

What is a Blakemore tube?

A

NG tube with 2 balloons;
1 esophageal
1 gastric

tension should be held on it with 250-500g

81
Q

What else do you need if the patient has a Blakemore tube?

A

secure airway*

82
Q

What is the time limit for a Blakemore Tube?

A

should not be in place >6 hours

83
Q

What is a mesocaval shunt?

A

A portosystemic shunt between the superior mesenteric vein and the inferior vena cava to reduce portal hypertension

84
Q

What is esophagitis?

A

Inflammation of the lining of the esophagus may be caused by gastric acid, ingested chemicals, immune reactions, and infectious agents

85
Q

What are causes of esophagitis?

A
  • gastric acid
  • ingested chemicals
  • immune reactions
  • infectious agents
86
Q

What is reflux esophagitis?

A

Esophageal mucosa exposed to gastric acid over time will develop
inflammation and injury

87
Q

What are causes of reflux esophagitis?

A

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
Q

What is the pathophysiology of reflux esophagitis?

A
  • Irritation leads to mucosa inflammation
  • Infiltrated with eosinophils and neutrophils
  • Can lead to ulcerations, infections, and perforation
89
Q

What are symptoms of reflux esophagitis?

A
  • heartburn
  • dysphagia
  • regurgitation of sour gastric contents
  • Chest pain which can be mistaken for heart disease
90
Q

What is Barrett esophagus?

A

complication of chronic GERD

  • Metaplastic conversion of normal squamous esophageal epithelium to columnar epithelium

→ may involve a genetic predisposition (TP53 mutations)

91
Q

Barrett esophagus is a precursor to ___.

A

adenocarcinoma

92
Q

When is Barrett esophagus diagnosed?

A

often at advanced stages

93
Q

What is eosinophilic esophagitis?

A
  • inflammatory condition in response to allergens in food (milk, soy)
94
Q

What is eosinophilic esophagitis associated with?

A

other forms of atopy

→ atopic dermatitis
→ allergic rhinitis
→ asthma

95
Q

What is the pathophysiology of eosinophilic esophagitis?

A

Eosinophils are present in the esophageal mucosa, typically in far greater
numbers than in GERD

→ May also include upper and mid esophagus

96
Q

Symptoms of eosinophilic esophagitis:

A
  • dysphagia

- intolerance of foods with the allergen

97
Q

What is the treatment for eosinophilic esophagitis?

A
  • PPIs are of limited efficacy
  • exclusion of offending allergen
  • systemic steroids
98
Q

What are 3 stomach pathophysiologies?

A
  1. gastritis [acute, chemical, stress-related, H.pylori]
  2. peptic ulcer disease
  3. neuroendocrine tumors
99
Q

What is gastritis?

A

inflammation of the gastric mucosa

100
Q

What is the cause of gastritis?

A
  • Exposure to acid and other injurious agents

* An imbalance between damaging factors and mechanisms that protect the stomach lining from these agents

101
Q

What are symptoms of acute gastritis?

A
  • May be asymptomatic
  • Epigastric pain, nausea, and vomiting
  • Ulceration and hemorrhage, resulting in hematemesis (vomiting of blood)
102
Q

What is the pathology of acute gastritis?

A
  • 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
Q

In acute gastritis, where are neutrophils?

A

within the epithelial layer

104
Q

What are common causes of chemical gastritis?

A
  • NSAIDs
  • Uremia & infection by H. pylori
  • Chemical exposures
105
Q

How do NSAIDs cause chemical gastritis?

A

Inhibit production of prostaglandins, which normally stimulate mucin and bicarbonate secretion and mucosal blood flow

106
Q

How does uremia & infection by H.pylori cause chemical gastritis?

A

may inhibit gastric bicarbonate transporters

107
Q

How do chemical exposures cause chemical gastritis?

A

Acids and alkalis, alcohol, and chemotherapeutic drugs, may directly injure the gastric mucosa

108
Q

Who is prone to developing stress-related gastritis?

A

patients with:

  • severe trauma
  • burns
  • extensive surgery
  • critical illness
109
Q

Pathology of stress-related gastritis:

A
  • 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
Q

What is H.pylori?

A

a spiral-shaped bacillus detectable in gastric mucosal biopsies from many patients with duodenal ulcer and chronic gastritis

111
Q

H. pylori gastritis is common in:

A
  • children
  • crowded living conditions
  • poor sanitation
112
Q

H. pylori infection is associated with:

A

an increased risk of gastric carcinoma

113
Q

Pathology of H.pylori:

A
  • 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
Q

What are symptoms of H.pylori gastritis:

A

typical signs of gastritis (pain, N/V)

115
Q

How is H.pylori gastritis diagnosis:

A
  • 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
Q

What is peptic ulcer disease?

A

A benign ulcer composed of granulation tissue and necrotic cell debris and inflammatory cells resting on a fibrous scar

117
Q

peptic ulcer disease results from:

A

excess gastric acid and an impaired mucosal defense

often the consequence of H. pylori infection and chronic NSAID use

118
Q

What anatomical location & age range is peptic ulcer disease most common:

A

More frequent in the duodenum than in the stomach and seen in
middle-age or older adults

119
Q

What is the treatment for gastritis?

A
  • antacids
  • H2 receptor antagonists
  • proton pump inhibitors
  • prostaglandin analogues
120
Q

Antacids as treatment for gastritis:

A
  • aluminum hydroxide
  • magnesium hydroxide (e.g., Maalox, Mylanta)
  • calcium carbonate (Tums)

• symptomatic relief of dyspepsia

121
Q

H2 receptor antagonists for treatment of gastritis:

A
  • cimetidine
  • ranitidine
  • famotidine
  • nizatidine

• inhibit basal and stimulated gastric acid secretion

122
Q

Proton pump inhibitors for treatment of gastritis:

A
  • omeprazole
  • esomeprazole
  • lansoprazole
  • rabeprazole
  • pantoprazole

• covalently bind and irreversibly inhibit hydrogen potassium–adenosine triphosphatase (H + ,K + -ATPase)

123
Q

Prostaglandin analogues for treatment of gastritis:

A
  • misoprostol

• enhance mucosal bicarbonate secretion, stimulate mucosal blood flow, and decrease mucosal cell turnover

124
Q

Polyps:

A

inflammatory abnormal tissue when cells grow and divide more they should or do not die when they should

• frequent incidental findings in endoscopies

125
Q

When are polyps usually found:

A

frequently an incidental findings in endoscopies

126
Q

Adenoma:

A

abnormal tissue that may serve as precursors for cancers

127
Q

What type of epithelia dysplasia is found in adenomas?

A

varying degrees

128
Q

What is the most common malignancy of the stomach?

A

adenomas;

  • idiopathic
  • familial adenomatous polyposis syndrome
  • H.pylori - induced
  • Epstein-Barr virus (EBV) infection
129
Q

Do adenomas spread or stay localized?

A

can spread locally to involve the duodenum, pancreas & retroperitoneum

130
Q

Where do adenomas spread?

A

locally to duodenum, pancreas, & retroperitoneum

131
Q

What is a neuroendocrine tumor?

A

a type of tumor that grows from neuroendocrine cells

132
Q

What do neuroendocrine cells do?

A

send and receive messages through hormones to help the body function

133
Q

Where are neuroendocrine cells found?

A

in all organs throughout the body

134
Q

Do carcinoid tumors grow slow or fast?

A

slow

135
Q

Where are most carcinoid tumors found?

A

75% are found in the GI tract (often in the small intestine)

25% are found in the lungs

136
Q

What type of neuroendocrine tumors rarely spread?

A

foregut neuroendocrine tumors

[stomach, duodenum, esophagus]

137
Q

Where are foregut neuroendocrine tumors?

A
  • stomach
  • duodenum
  • esophagus
138
Q

What type of tumor increases gastric acid production, causing ulcers?

A

gastrinomas

139
Q

What is the cause of Zollinger-Ellison syndrome?

A

gastrinomas that increase gastric acid production, leading to ulcers

140
Q

Where are midgut carcinoid tumors?

A

small intestine

141
Q

What are characteristics of midgut carcinoid tumors?

A

located in the small intestine, often multiple and aggressive

142
Q

Where are hindgut carcinoid tumors located?

A

appendix and colon

143
Q

What are characteristics of hindgut tumors?

A

usually incidental and benign

N935 Advanced Pathophysiology (9 decks)

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