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SMP - APP Part 1 > Lectures 13 & 14 - GI Pathophysiology I & II > Flashcards

Lectures 13 & 14 - GI Pathophysiology I & II Flashcards

1
Q

What are the 5 clinical manifestations of GI pathophysiologies?

A
  1. Anorexia
  2. Nausea
  3. Vomiting (emesis)
  4. Hematemesis
  5. Melena: tarry or occult
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2
Q

What does anorexia mean?

A

Loss of appetite

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3
Q

What kind of mechanism is vomiting? Describe it.

A

Reflex

Vomiting center of the brain regulated by:

  1. The chemoreceptor trigger zone in the 4th ventricle of the brain in contact with blood and CSF
  2. Cerebral cortex
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4
Q

What is hematemesis?

A

Blood in vomit

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5
Q

How to tell where the blood is from in vomit?

A

Higher in GI: more red

Lower in GI: darker red

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6
Q

What is melena?

A

Blood in stool

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7
Q

How to tell where the blood is from in stool? What is this called?

A

Higher in GI: darker red = tarry

Lower in GI: more red

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8
Q

What does occult melena mean?

A

Blood in stool that is not grossly visible

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9
Q

Definition of diarrhea?

A

Passage of more than 200g per day of feces

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10
Q

4 types of diarrhea?

A
  1. Osmotic
  2. Secretory
  3. Inflammatory
  4. Noninflammatory
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11
Q

Diarrhea consistency?

A

Depends on origin

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12
Q

Example of secretory diarrhea?

A

Cholera

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13
Q

What is an inflammatory diarrhea?

A

Diarrhea with inflammation of the walls of the GIT

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14
Q

2 examples of inflammatory diarrhea?

A
  1. Ulcerative colitis

2. Crohn’s disease

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15
Q

Definition of constipation? What to note?

A

Infrequent passage of stool (precise infrequency not defined as what might be normal for one person might be abnormal for another0

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16
Q

Causes of constipation?

A
  1. Could be a primary problem
  2. Problem association with another disease condition:
    - Failure to respond to the urge to defecate
    - Inadequate dietary fiber
    - Inadequate fluid intake
    - Weakness of the abdominal muscles
    - Inactivity
    - IBS
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17
Q

Why does inactivity cause constipation?

A

Decreased GIT motility => increased water reabsorption

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18
Q

Functions of upper esophageal sphincter?

A
  1. Ensures air breathed in does not enter the GIT

2. Ensures food does not enter the trachea

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19
Q

Functions of lower esophageal sphincter?

A
  1. Ensures no regurgitation of gastric contents in the esophagus
  2. Regulates the flow of food from the esophagus into the stomach
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20
Q

Are esophageal sphincters normally in a tonic state?

A

YUP

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21
Q

What is the LES made of?

A
  1. Circular smooth muscle in the esophageal wall
  2. Reinforced by esophageal hiatus of the diaphragm
  3. Oblique muscles of the stomach
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22
Q

What is the UES made of?

A

Skeletal muscles sling around the esophagus:
1. Cricopharyngeal mucles
+ 3 other skeletal muscles

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23
Q

How does the UES stay closed?

A

Receives constant autonomic innervation to remain constricted, which stops for relaxation

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24
Q

How does the LES stay closed?

A

Normally tonically constricted without need for constant innervation, and relaxes when innervated to do so

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25
Q

What is esophageal manometry? How does it work?

A

Test used to measure the function of the UES and LES: long wire inserted in the esophagus to the stomach

Force transducers are along the wire to measure the force (in mmHg) of the esophagus during swallowing

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26
Q

What is a normal reading using esophageal manometry?

A
  1. UES: normal pressure is 100 mmHg/during swallowing the pressure drops to 0 (complete relaxation) and then goes back higher than 100 and then back to normal
  2. Rest of esophagus: normal pressure is 0 mmHg/pressure goes up as bolus goes down = wave of peristalsis moving the bolus down
  3. LES: normal pressure is 40 mmHg/during swallowing the pressure drops to 0 (complete relaxation) and then goes back higher than 40 and then back to normal
  4. Stomach: normal pressure is >0 mmHg
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27
Q

Significance of normal gastric pressure > 0 mmHg?

A

Without a LES, there would be regurgitation since the pressure in the esophagus IS 0 mmHg

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28
Q

4 pathologies associated with swallowing?

A
  1. Dysphagia
  2. Odnyphagia
  3. Pyrosis
  4. Achalasia
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29
Q

What does dysphagia mean? 2 types?

A

= difficulty swallowing

  1. Oropharyngeal dysphagia: cannot get the food from the mouth to the esophagus
  2. Esophageal dysphagia
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30
Q

How many cranial nerves associated with swallowing reflex?

A

Many

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31
Q

In what patients is dysphagia common? Why?

A

Stroke victims as cranial nerves are affected

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32
Q

What is odnyphagia? Causes?

A

Painful swallowing

Causes: infections, cancer, strictures

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33
Q

What is pyrosis?

A

Heart burn

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34
Q

What is achalasia?

A

Failure of LES to relax when swallowing

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35
Q

Treatment for prominent cricopharyngeus?

A

Surgery to de-innervate or remove the muscle

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36
Q

What 2 factors increase relaxation of the LES?

A
  1. Gastric distension

2. High fat meals

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37
Q

What 2 factors increase relaxation of the LES?

A
  1. Gastric distension

2. High fat meals

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38
Q

Describe the innervation of the LES. Which innervation causes relaxation?

A
  1. Vagus nerve
  2. SNS from the sympathetic chain ganglia in the thorax, which then synapses in the celiac ganglion
  3. ***Other innervation (interneuron) that is unknown
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39
Q

Describe the manometry reading of a patient with achalasia.

A
  1. Loss of normal peristalsis
  2. LES pressure remains high during swallowing
  3. High resting tone (=basal pressure) of the LES
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40
Q

Diagnostic tool for achalasia?

A

Barium swallow with imaging

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41
Q

Effects of long-term achalasia?

A
  1. Dilation of the esophagus
  2. Sigmoid or megaesophagus
  3. Weight loss and malnutrition
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42
Q

Achalasia treatment? Side effect?

A

Surgical opening of the LES to remove its muscles

Side effect: GERD

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43
Q

Achalasia cause?

A

Unknown

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44
Q

What is GERD?

A

= Gastroesophageal Reflux Disease

  1. Incompetent LES
  2. Delayed gastric emptying
  3. Acid hypersecretion
  4. Decreased salivation: further worsens the delayed gastric emptying and not enough esophageal protection from gastric contents
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45
Q

Which esophageal sphincter opens for longer during swallowing? Implication?

A

LES

Implication: gastric reflux is normal to a certain extent

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46
Q

What can cause an incompetent LES? Which is the hardest to treat?

A
  1. Weak basal LES pressure
  2. Inadequate LES response to increased abdominal pressure (should constrict to avoid regurgitation) (e.g. coughing)
  3. Inadequate LES response to gastric contractions
  4. ***Transient relaxation of the LES (for unknown reason)
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47
Q

Anatomic abnormality causing GERD?

A

Hiatal hernia

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48
Q

Pathophysiology of GERD?

A

Acid refluxes into distal esophagus => disruption of tight junctions => acid reaches intercellular space => cell edema and death => mucosal inflammation

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49
Q

4 symptoms of GERD?

A
  1. Reflux involves mucosal injury to the esophagus, hyperemia, and inflammation
  2. Heartburn:
    - 30-60 min after eating
    - Made worse by bending at the waist due to increased abdominal pressure
    - Most often occurs at night because laying down and because of hormones relaxing the LES
  3. Belching and chest pain
  4. Respiratory symptoms: wheezing, chronic cough, and hoarseness
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50
Q

4 effects of chronic GERD?

A
  1. Persistent reflux: cycle of mucosal damage that causes hyperemia, edema, and erosion of the luminal surface
  2. Strictures: narrowing of the esophagus due to inflammation causing scarring
  3. Barrett’s esophagus: normal squamous mucosa becomes metaplastic columnar mucosa (same as stomach epithelial lining) to handle the high acid load
  4. Increased risk for cancer due to Barrett’s esophagus
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51
Q

What is hyperemia?

A

An excess of blood in the vessels supplying an organ

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52
Q

Treatments for GERD?

A
  1. Conservative measures first: avoidance of positions and conditions that increase GERD:
    - Avoid large meals and foods that reduce LES tone (e.g. caffeine, fats, chocolate)
    - Avoid smoking and alcohol
    - Have meals eaten sitting up
    - Avoid bending for long periods of time
    - Weight loss
  2. Aggressive treatments:
    - Block gastric acid secretion
    - Drugs that increase motility
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53
Q

What protects the stomach from its acidity and peptic enzymes? What are these regulated by?

A
  1. The gastric mucosal barrier: water-repellent hydrophobic layer with bicarb in the mucus
  2. High restitution: cell turnover
  3. High gastric blood flow: washes away gastric acid

=> regulated by prostaglandins

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54
Q

Why is stomach cancer so lethal?

A

Because the stomach has a great distention ability so tumors go unnoticed for a long time => usually asymptomatic until late in its course

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55
Q

Life-span of gastric cell?

A

3-7 days

56
Q

What is gastritis? 2 types?

A

= Damage to the gastric mucosa with acute inflammation, necrosis, and hemorrhage

  1. Acute gastritis
  2. Chronic gastritis
57
Q

4 causes of chronic gastritis?

A
  1. Autoimmune gastritis
  2. Multifocal atrophic gastritis
  3. Chemical gastropathy
  4. Helicobacter pylori gastritis (bacterial infection)
58
Q

2 causes of acute gastritis?

A
  1. Chronic NSAID use

2. Helicobacter pylori gastritis (bacterial infection)

59
Q

What can lead to a peptic ulcer?

A
  1. Increased damage to the stomach
  2. Impaired gastric defenses (e.g. NSAID use, ischemia, shock)

OR BOTH

60
Q

How does Helicobacter Pylori infection cause gastritis?

A
  1. Flagella allows the bacteria to be mobile in mucus
  2. Urease enzyme: urea + H2O => CO2 + ammonia => elevates pH by neutralizing acid => allows bacteria to approach gastric epithelium + damages the epithelium + allows gastric acid and enzymes to access the epithelium
  3. Mucinase damages the gastric mucosa
  4. Adhesins enhance bacterial adherence to foveolar cells
  5. Toxins may be involved in disease progression (CagA)
61
Q

What can increase damage to the stomach? 6 factors.

A
  1. H. pylori
  2. NSAIDs
  3. Tobacco
  4. Alcohol
  5. Gastric hyperacidity
  6. Duodenal-gastric reflux
62
Q

In what patients are H. pylori infections decreasing? Increasing? Why?

A

Decreasing in young patients

Increasing in the elderly

BECAUSE

63
Q

Treatment for acute gastritis caused by H. pylori infection?

A

Usually resolves on its own

64
Q

Complication of acute gastritis caused by H. pylori infection? How does this usually occur?

A

Peptic ulcer disease

When infection happens in conjunction with NSAID use or other factors

65
Q

What is peptic ulcer disease?

A

Group of ulcerative disorders that occur in the upper GIT where the submucosal layer is exposed to gastric contents causing autodigestion

66
Q

Most common 3 causes of peptic ulcer disease?

A
  1. H. pylori infection
  2. Increased acid and/or pepsin (and gastrin)
  3. Decreased bicarb
67
Q

2 places in GIT where we usually find peptic ulcer disease? Which is more common?

A
  1. Stomach antrum (more in elderly patients)

2. ***Duodenal bulb

68
Q

Why is it called PEPTIC ulcer disease?

A

Pepsin damage increases the acid damage

69
Q

Describe the progression from gastritis to peptic ulcer.

A

Acid in gastric mucosa =>

  1. Pepsin conversion => further erosion of mucosa and bleeding
  2. Histamine formation => increased gastric acid secretion

=> ULCERATION

70
Q

Symptom of duodenal ulcer?

A

Pain between meals and in the early morning

71
Q

Why does smoking increase risk of peptic ulcers?

A

Smoking increases acid production

72
Q

Why do NSAIDs increase risk of peptic ulcers?

A

Inhibit prostaglandin synthesis which normally increase mucosal blood flow and stimulate HCO3- secretion

73
Q

Symptom of gastric ulcer?

A
  1. Pain, but not associated with eating
  2. Anorexia
  3. Vomiting
  4. Weight loss
74
Q

Which ulcers tend to be chronic: duodenal or gastric?

A

Gastric

75
Q

What are stress ulcers?

A

Acute peptic ulcer related to severe illness, neural injury, or systemic trauma that occurs at multiple sites

76
Q

2 subtypes of stress ulcers? Describe each.

A
  1. Ischemic ulcers: happen within hours of event (hemorrhage, heart failure, severe burns: Curling ulcer)
  2. Cushing ulcers: develop as a result of a head trauma/brain surgery causing decreased mucosal blood flow and overstimulation of vagal nuclei causing hypersecretion of acid
77
Q

Is stomach cancer common? What to note?

A

NOPE - only 3% of malignancies

BUT most common fatal cancer in the US

78
Q

What patients get stomach cancer?

A
  1. Genetic predisposition
  2. More common in men
  3. More common for Type A blood patients
  4. Carcinogenic factors: N-nitroso compounds and benzopyrene in smoked meats
  5. Infection with H. pylori: appears to serve as a co-factor
79
Q

Symptoms of stomach cancer? What to note?

A

VAGUE SYMPTOMS:

  1. Indigestion
  2. Anorexia
  3. Weight loss
  4. Vague pain
  5. Vomiting
80
Q

What is reabsorbed in the duodenum?

A
  1. Iron
  2. Calcium
  3. Folic acid
81
Q

What is reabsorbed in the jejunum?

A
  1. Carbohydrates
  2. Proteins
  3. Fats
82
Q

What is reabsorbed in the ileum?

A
  1. Bile salts

2. Vitamin B12

83
Q

What is irritable bowel syndrome (IBS)?

A

Functional gastrointestinal disorder characterized by abdominal pain and constipation with or without mucous discharge and episodic diarrhea

84
Q

Cause of IBS?

A

Believed to be the result from dysregulation of intestinal motor and sensory function modulated by CNS causing increased motility and abnormal intestinal contraction in response to psychological and physiologic stress

Overall abnormal myoelectric and motor activities in the GIT

85
Q

What kind of diarrhea does IBS cause?

A

Non-inflammatory diarrhea

86
Q

4 symptoms of IBS?

A
  1. Abdominal pain relieved by defecation
  2. Altered frequency of bowel movement
  3. Sensation of incomplete evacuation
  4. Passage of mucus upon defection
87
Q

What is inflammatory bowel disease (IBD)?

A

Crohn’s disease and ulcerative colitis that are both autoimmune

88
Q

What are commonalities between Crohn’s disease and ulcerative colitis?

A
  1. Inflammation of the bowel
  2. Lack of confirming evidence of a proven causative agent
  3. Pattern of familial occurrence
  4. Accompanied by systemic manifestation(s)
89
Q

Possible 4 causes of IBD?

A
  1. Hereditary predisposition
  2. Epithelial defects in intestinal epithelial tight junction barrier allowing bacteria to enter causing an immune response
  3. Microbiota (can be fixed with fecal transplant)
  4. Environmental triggers
90
Q

6 possible systemic manifestations of IBD?

A
  1. Arthritis: spine, sacroiliac joint (most common), and large joints of the arms and leg
  2. Inflammatory conditions of the eye
  3. Skin lesions: erythema nodosum
  4. Hypercoagulability of the blood
  5. Stomatitis
  6. Autoimmune anemia
91
Q

What is stomatitis?

A

Ulcerations of mucosal surfaces (e.g. palate, anus)

92
Q

What is erythema nodosum?

A

Inflammation of blood vessels which can burst

93
Q

Effect of IBD on nutrient absorption?

A

Impaired due to the inflammation of the GIT walls

94
Q

Describe Crohn’s disease. 5 features.

A
  1. Can affect any area from the mouth to the anus with skip lesions (instead of continuous)
  2. Recurrent granulomatous type of inflammatory response: sharply demarcated granulomatous lesions that are surrounded by normal appearing mucosal tissue (hallmark)
  3. Progressive, relentless, and disabling
  4. All layers of bowel involved: submucosal most involved
  5. Ulcerations can produce longitudinal and transverse inflammatory fissures that extend into the lymphatics
95
Q

Clinical course of Crohn’s disease?

A

Often variable: periods of exacerbation and remission

96
Q

5 symptoms of Crohn’s disease?

A

Symptoms are often related to the location of the lesions (e.g. nutritional deficiencies)

  1. Diarrhea with small amounts of blood or none
  2. Colicky pain
  3. Weight loss
  4. Fluid and electrolyte disorders
  5. Malaise
97
Q

Pathophysiological pathway of Crohn’s disease?

A

Dysfunctional intestinal epithelium => allows for frequent exposure to unknown antigens => overly aggressive TH1 response => cytokines recruit inflammatory cells to the intestinal mucosa (including macrophages with secrete more cytokines to further the TH1 response) => amplified and sustained immune response => transmural GIT inflammation

98
Q

Describe ulcerative colitis. 5 features.

A
  1. Nonspecific inflammatory condition confined to the rectum and colon
  2. Affects primarily the mucosal layer
  3. Affected site tends to be continuous
  4. Leads to the formation of pinpoint mucosal hemorrhages, which can become necrotic and ulcerate
  5. As a result of the inflammatory process, the mucosal layer develops tongue-like projections that resemble polyps
99
Q

4 symptoms of ulcerative colitis?

A
  1. Diarrhea with blood and mucus since the mucosal layer is affected
  2. Mild abdominal cramping
  3. Anorexia
  4. Weakness
100
Q

3 treatments for IBD?

A
  1. Broad-spectrum antibiotics (which supports the microbiota theory)
  2. Immunosuppressive agents
  3. Surgery
101
Q

Is the terminal ileum affected in Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: commonly

2. Ulcerative colitis: seldom

102
Q

Is the colon affected in Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: usually

2. Ulcerative colitis: always

103
Q

Is the rectum affected in Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: seldom

2. Ulcerative colitis: usually

104
Q

Depth of inflammation in Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: transmural

2. Ulcerative colitis: shallow, mucosal

105
Q

Are fistulae seen in Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: commonly

2. Ulcerative colitis: seldom

106
Q

Effect of surgery on Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: disease often returns

2. Ulcerative colitis: cure

107
Q

Effect of smoking on Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: increases the risk of the disease

2. Ulcerative colitis: decreases the risk of the disease and helps as a therapeutic agent

108
Q

Is sclerosis of the bile duct seen in Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: NOPE

2. Ulcerative colitis: commonly

109
Q

Describe distribution of the inflammation in Crohn’s disease and ulcerative colitis.

A
  1. Crohn’s disease: patchy

2. Ulcerative colitis: continuous

110
Q

Are patients with Crohn’s disease and ulcerative colitis at risk of getting GIT cancer?

A
  1. Crohn’s disease: lower risk

2. Ulcerative colitis: higher risk

111
Q

Biopsy results for patients with Crohn’s disease and ulcerative colitis?

A
  1. Crohn’s disease: non-peri-intestinal crypt granulomas

2. Ulcerative colitis: crypt abscesses and cryptitis

112
Q

What is a fistula?

A

Abnormal connection between body parts

113
Q

What 4 kinds of fistulae seen with Crohn’s disease?

A
  1. Between 2 portions of the GIT => decreases absorptive ability
  2. Between GIT and abdominal wall
  3. Between GIT and bladder
  4. Between GIT and vagina
114
Q

Why don’t we see fistulae with ulcerative colitis?

A

Because the GIT inflammation is shallow, not transmural

115
Q

What is appendicitis? Cause?

A

Appendix becomes inflamed, swollen, and gangrenous, and it eventually perforates if not treated

Cause: thought to be related to intraluminal obstruction with a fecalith (hard piece of stool) or twisting

116
Q

What is the appendix attached to?

A

Cecum

117
Q

Why is appendix perforation dangerous?

A

Chyme released in peritoneal space => peritonitis

118
Q

Describe the pathway of the pathophysiology of appendicitis.

A

Occlusion of lumen => continued mucosal secretions => increased intramural pressure => limit venous flow => hypoxia => mucosa ulcerates => bacterial invasion (includes gas) => further increase in intraluminal pressure => arterial circulation thrombosed => gangrene and perforation

119
Q

What is diverticular disease? Location? In what patients is it common?

A

Herniations/outpouchings of mucosa in between the circular muscle layers of the colon wall

Location: especially the sigmoid colon

Common in the elderly in Western societies (almost non-existent in many African nations)

120
Q

Difference between diverticulum, diverticulosis, diverticulitis, diverticular disease?

A
  1. Diverticulum = herniation/outpouching of the mucosa through the muscle layers of the colon wall
  2. Diverticulosis = multiple diverticula
  3. Diverticulitis = inflammation and/or gross or microscopic perforation of diverticulum
  4. Diverticular disease = symptoms of diverticulitis
121
Q

3 possible causes of diverticular disease?

A
  1. Dietary factors in Western societies
  2. Decrease in physical activity
  3. Aging
122
Q

Why is diverticular disease mainly occurring in the sigmoid colon?

A

Because of the Law of La Place:

T = P x R
T = tension in the wall of a cylinder
P = pressure within
R = radius

=> T is constant in the circular muscle of the colon, so intraluminal pressure is greatest when lumen is narrowest => sigmoid colon!

123
Q

What causes the progression from diverticulosis to diverticulitis?

A

Same as for appendicitis

124
Q

Symptoms of diverticular disease?

A
  1. Abdominal pain
  2. Blood in diarrhea
  3. Bleeding or infection in peritoneal cavity
125
Q

Treatment for diverticular disease?

A

Surgery

126
Q

What is malabsorption syndrome?

A

Constellation of symptoms arising from multiple causes and shared between patients
with conditions that diffusely affect the small intestine and reduce its absorptive functions

127
Q

5 examples of causes of malabsorption syndrome?

A
  1. Celiac Sprue
  2. Crohn’s disease
  3. Bowel resection
  4. Diverticular disease
  5. IBS
128
Q

8 symptoms of malabsorption syndrome?

A
  1. Diarrhea
  2. Steatorrhea
  3. Flatulence
  4. Bloating
  5. Abdominal pain, cramps, and distention
  6. Weakness, muscle wasting, weight loss
  7. Easy bruising and bleeding
  8. Bone pain
129
Q

Why does malabsorption syndrome cause flatulence?

A

Because the bacteria in the gut have more nutrients and produce more gas

130
Q

Why does malabsorption syndrome cause easy bruising and bleeding?

A

Poor clotting and coagulation due to iron vitamin deficiencies (B12, K)

131
Q

Why does malabsorption syndrome cause bone pain?

A

Calcium deficiency => PTH release => bone breakdown

132
Q

What is Celiac Sprue?

A

Rare chronic disease in which there is a characteristic mucosal lesion of the small intestine causing impaired nutrient absorption due to loss of absorptive villi

133
Q

Treatment for Celiac Sprue?

A

Remove gluten from diet

134
Q

Cause of Celiac Sprue?

A

Believed to be a immunologic response to gluten

135
Q

What is gluten?

A

Casein protein found in wheat

136
Q

Pathophysiology of Celiac Sprue?

A

Gluten broken down into gladin => gladin enters GIT wall => immunologic response => microvilli destruction on GIT epithelial cells

137
Q

Other feature of GIT in Celiac Sprue patients?

A

Leaky tight junctions between epithelial cells of the GIT

SMP - APP Part 1 (8 decks)

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