Gastrointestinal disorder Flashcards

1
Q

what is dyspepsia?

A

Defined as an episodic or persistent discomfort or pain in upper abdomen that may be accompanied of a sensation of fulness, bloating, heartburn, nausea, vomiting, belching, or burping.

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2
Q

what is functional dyspepsia?

A

Functional dyspepsia (Rome IV criteria):
Prescence of one or more of the following:
Bothersome postprandial fullness
Bothersome early satiation
Bothersome epigastric pain
Bothersome epigastric burning

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3
Q

what is most common cause of dyspepsia?

A

Functional dyspepsia (most common cause; results from interaction between increased visceral afferent sensitivity, delayed gastric emptying, and psychosocial stressors).
Food or drug intolerance (eating too much, too quickly, high-fat meals, eating during stress, drinking too much coffee, alcohol, etc.).
Peptic ulcer disease, GERD , H. pylori infection, cancer , pancreatic disease, biliary tract disease, pregnancy.
Other (gastroparesis, thyroid disease, chronic kidney disease, hernias, chronic intestinal ischemia).

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4
Q

what are the different types of causes of constipation with examples for each?

A

Mechanical: obstruction (malignancy; internal or external masses), strictures.

Anatomical: fissure, anismus, rectocele.

Metabolic: hypercalcemia inhibits sodium channels affecting neuronal excitation and reducing the tone and excitability of the bowel smooth muscle. Other hypomagnesemia.

Endocrine: hypothyroidism inhibits Cl−/HCO3− anion exchange and reduces intestinal motility. Deposition and accumulation of glycosaminoglycans (hyaluronic acid) that impairs motility. Clinically evident as reduced peristalsis, may produce distension, pain, etc. other diabetic autonomic neuropathy,

Neurological: multiple sclerosis leads to altered autonomic nerve response and reduced reflex responses after a meal. Other Parkinson disease.

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5
Q

what are the classes of constipation?

A

Rheumatological: scleroderma produces deposition and accumulation of collagen in GIT mucosal leading to fibrosis, reduced motility, atrophy pf smooth muscle and reduced ability to contract.

Pelvic floor dyssynergia: lack of relaxation of external anal sphincter and puborectalis muscle leads to an ineffective feces’ evacuation.

IBS-C: Reduced colonic motility due to impaired interaction between enteric and central nervous system (mechanism unknown; many pathways).

Drugs: opioids bind to receptors on gut wall and inhibit excitatory pathways within enteric nervous system. Anticholinergics inhibit action of parasympathetic nervous system.

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6
Q

what is nausea and what is vomiting?

A

Nausea: vague, intensely disagreeable sensation of sickness or “queasiness”.

Vomiting: expulsion of gastric contents following spasmodic respiratory and abdominal movements.

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7
Q

what is regurgitation and what is rumination?

A

Regurgitation: effortless reflux of liquid or food stomach contents.

Rumination: chewing and swallowing of food that is regurgitated volitionally after meals.

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8
Q

what are the complications of vomiting?

A

Complications:
Dehydration, hypokalemia, metabolic alkalosis.

Aspiration (aspiration pneumonia, lung abscess).

Rupture of the esophagus (Boerhaave’s syndrome).

Bleeding secondary to a mucosal tear at the gastroesophageal junction (Mallory-Weiss syndrome).

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9
Q

what composes the vomiting center?

A

Vomiting center (medulla) is composed of the area postrema, nucleus tractus solitarius, and the central pattern generator.

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10
Q

what is the pathophysiology of vomiting?

A

Receives stimuli from:
Visceral afferent fibers (serotonin receptors; vagus nerve sending signals of distension, irritation, infection).

Vestibular system (fibers have histamine H1 and muscarinic receptors M1).

Amygdala (may send signals in anticipation to events (chemotherapy).

Chemoreceptor trigger zone (in area postrema of medulla, outside blood brain barrier).
Stimulated by drugs, chemotherapeutic agents, toxins, hypoxia, uremia, acidosis, and radiation therapy.

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11
Q

what are the 2 types of dysphagia?

A

Oropharyngeal dysphagia:
Neurological: cerebrovascular accidents, brainstem infarctions with cranial nerve involvement, basal ganglia disorders (Parkinson disease), head and neck injuries/surgery, multiple sclerosis, brain tumor, botulism, amyotrophic lateral sclerosis, degenerative cervical spine disease.
Muscular: polymyositis, muscular dystrophy, and myasthenia gravis.
Anatomical: Zenker diverticulum, enlarged thyroid, esophageal web, tumors, abscess, external compression by aortic aneurysm.

Esophageal dysphagia:
Mechanical obstruction: Schatzki ring, esophageal stricture or carcinoma, eosinophilic esophagitis.
Motility disorders: esophageal spasm, achalasia and scleroderma.
Rheumatologic: Sjogren syndrome, systemic lupus erythematosus, systemic sclerosis (CREST syndrome), rheumatoid arthritis.
Drugs: due to xerostomia, changes in esophageal motility, pill esophagitis or GERD.

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12
Q

what are the causes of oropharyngeal dysphagia?

A

Neurological: cerebrovascular accidents, brainstem infarctions with cranial nerve involvement, basal ganglia disorders (Parkinson disease), head and neck injuries/surgery, multiple sclerosis, brain tumor, botulism, amyotrophic lateral sclerosis, degenerative cervical spine disease.

Muscular: polymyositis, muscular dystrophy, and myasthenia gravis.

Anatomical: Zenker diverticulum, enlarged thyroid, esophageal web, tumors, abscess, external compression by aortic aneurysm.

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13
Q

what are the causes of esophageal dysphagia?

A

Mechanical obstruction: Schatzki ring, esophageal stricture or carcinoma, eosinophilic esophagitis.

Motility disorders: esophageal spasm, achalasia and scleroderma.

Rheumatologic: Sjogren syndrome, systemic lupus erythematosus, systemic sclerosis (CREST syndrome), rheumatoid arthritis.

Drugs: due to xerostomia, changes in esophageal motility, pill esophagitis or GERD.

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14
Q

what is achalasia?

A

Rare functional disorder resulting from progressive degeneration of ganglion cells in the myenteric plexus in the esophageal wall, leading to failure of relaxation of the lower esophageal sphincter (LES), accompanied by a loss of peristalsis in the distal esophagus.

Primary or idiopathic achalasia (unknown etiology).

Secondary achalasia: due to diseases that cause esophageal motor or abnormalities similar or identical to those of primary achalasia (Chagas disease, viral infections, malignant infiltration, etc.

Most frequent presentation: dysphagia for solids and liquids and regurgitation of bland undigested food or saliva. May have chest pain, heartburn (unresponsive to proton pump inhibitors), and difficulty belching.

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15
Q

what are the 2 forms of achalasia and their definitions?

A

Primary or idiopathic achalasia (unknown etiology).

Secondary achalasia: due to diseases that cause esophageal motor or abnormalities similar or identical to those of primary achalasia (Chagas disease, viral infections, malignant infiltration, etc.

Most frequent presentation: dysphagia for solids and liquids and regurgitation of bland undigested food or saliva. May have chest pain, heartburn (unresponsive to proton pump inhibitors), and difficulty belching.

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16
Q

what is the most frequent presentation of achalasia?

A

Most frequent presentation: dysphagia for solids and liquids and regurgitation of bland undigested food or saliva. May have chest pain, heartburn (unresponsive to proton pump inhibitors), and difficulty belching.

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17
Q

how does achalasia present?

A

Insidious onset and gradual progression. If rapid progression (think of cancer; pseudo achalasia).

Symptom onset 4.7 years before diagnosis (misdiagnosed as GERD).

Dysphagia for solids (91%) and liquids (85%).

Regurgitation of retained material (8%; especially while recumbent; risk of aspiration).

Patients try to vomit to relieve sensation of retrosternal fulness.

Pain is more common in younger patients (esophagus distends after some years).

Hiccups and retrosternal burning (symptoms like GERD).

Patients may adopt maneuvers to enhance esophageal emptying (lifting neck, throw shoulders back, eat more slowly).

May have mild weight loss and globus sensation.

18
Q

what is esophageal web, ring? and what is schatzki ring?

A

Web: thin (2-3 mm), eccentric, smooth extension of normal esophageal tissue consisting of mucosa and submucosa. Can occur anywhere; typically located in anterior area of proximal esophagus.
Associated with Plummer Vinson syndrome.

Ring: concentric, smooth, thin (3-5 mm) extension of normal esophageal tissue consisting of mucosa, submucosa, and muscle. Can be found anywhere along esophagus (usually in distal).

Schatzki ring is a web (only mucosa and submucosa) located at squamocolumnar junction (gastro esophageal junction) that marks the proximal margin of a hiatal hernia.

19
Q

what is plummer vinson syndrome? and what are its complication?

A

Chronic condition characterized by atrophic glossitis, upper esophageal webs (eccentric and often anterior), and iron deficiency anemia.

Rare condition most commonly seen in postmenopausal women in combination with other autoimmune diseases.

Presents with dysphagia to solid foods, cough, chocking, fatigue, nail changes, dizziness. On PE, atrophic glossitis, angular cheilitis, pallor, and koilonychia.

Barium studies: one (post-cricoid) or multiple esophageal webs; videofluoroscopy helps differentiate true webs from mucosal foldings.

Complications: esophageal squamous cell carcinoma and aspiration.

20
Q

what is Zenker diverticulum?

A

False diverticulum (contains only mucosa and submucosa) seen typically in middle-aged and older adults located in upper esophagus at Killian triangle (area of muscular weakness between cricopharyngeus and lower inferior constrictor muscles).

Pathogenesis: chronic increased pressure on Killian area (high pressures during swallowing or increased resistance due to abnormalities of the upper esophageal sphincter.

Presents with dysphagia, regurgitation, choking, halitosis, chronic cough and a palpable, fluctuant neck mass.

Complications: aspiration pneumonia, squamous cell carcinoma (up to 7%), ulceration, bleeding, high risk of iatrogenic perforation (during procedures).

21
Q

what is zenker diverticulum pathogenesis and how does it present?

A

Pathogenesis: chronic increased pressure on Killian area (high pressures during swallowing or increased resistance due to abnormalities of the upper esophageal sphincter.

Presents with dysphagia, regurgitation, choking, halitosis, chronic cough and a palpable, fluctuant neck mass.
Complications: aspiration pneumonia, squamous cell carcinoma (up to 7%), ulceration, bleeding, high risk of iatrogenic perforation (during procedures)

22
Q

what are zenker diverticulum complications?

A

Complications: aspiration pneumonia, squamous cell carcinoma (up to 7%), ulceration, bleeding, high risk of iatrogenic perforation (during procedures).

23
Q

what is Reflux Esophagitis and what are its most common symptoms?

A

Chronic relapsing condition in which the reflux of stomach content into the esophagus and beyond (larynx, lower respiratory tract) provokes symptoms and/or complications.

Most common symptoms: heartburn and regurgitation, but some extra-esophageal manifestations, such as asthma, chronic cough and laryngitis must be considered.

Pathogenesis: increase in transient lower esophageal sphincter relaxations or a decrease in lower esophageal sphincter pressure permits a reflux of acid, bile, pepsin and pancreatic enzymesthat generate esophageal mucosa injury.
Other contributing factors: Hiatal hernia, achalasia, and gastroparesis.
Asthma and chronic cough may result from thedirect contact of gastric acid with the upper airway, aspiration, or a vagovagal reflex elicited by acidification of the distal esophagus, leading to bronchospasm.

24
Q

what is reflux esophagitis pathogenesis?

A

Pathogenesis: increase in transient lower esophageal sphincter relaxations or a decrease in lower esophageal sphincter pressure permits a reflux of acid, bile, pepsin and pancreatic enzymesthat generate esophageal mucosa injury.

Other contributing factors: Hiatal hernia, achalasia, and gastroparesis.

Asthma and chronic cough may result from thedirect contact of gastric acid with the upper airway, aspiration, or a vagovagal reflex elicited by acidification of the distal esophagus, leading to bronchospasm.

25
Q

what is barret esophagus and what cancer can it develop into?

A

Complications:
Barret esophagus: metaplastic columnar epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus. Develops because of chronic GERD and predisposes to adenocarcinoma of the esophagus.

Esophageal adenocarcinoma.

26
Q

what is infectious esophagitis and what microorganisms causes it?

A

Infectious esophagitis: bacterial, viral, or fungal colonization of esophagus.

Risk factors: immunosuppression (HIV/AIDS, radiation, chemotherapy, organ transplant, corticosteroid, TNF inhibitors), broad spectrum antibiotics, decreased esophageal motility (diabetes, achalasia).
Use of antacids facilitates bacterial and fungal (candida) infections.

Bacterial: pathogens are difficult to isolate (generally polymicrobial & derived from normal oral microbiota).

Viral: cytomegalovirus infects endothelial cells and fibroblasts  large ulcers & odynophagia.

Fungal: Candida invades underlying tissue  white plaques (thrush) & increased neutrophils.

Complications: inflammation, ulceration, and mechanical stricture  dysphagia, odynophagia.

27
Q

what is eosinophilic esophagitis? What characterizes it and what other condition must it be distinguished from?

A

Immune mediated hypersensitivity to allergens (food or environmental) in genetically susceptible individuals.

Overexpression of eotaxin-3 gene; family history of atopy in 75%.

Combination of delayed Th-2 response and IgE mediated hypersensitivity.

Recruitment of eosinophils, mast cells mediated by Il-4, IL-5, IL-13.

Eotaxin-3 protein recruits eosinophils that degranulate & undergo cytolysis.

Must differentiate from GERD-induced eosinophilia (responds to PPI therapy).

Characterized by increased smooth muscle reactivity & epithelial hyperplasia & hypertrophy in esophagus.

28
Q

what are some risk factors for infectious esophagitis?

A

Risk factors: immunosuppression (HIV/AIDS, radiation, chemotherapy, organ transplant, corticosteroid, TNF inhibitors), broad spectrum antibiotics, decreased esophageal motility (diabetes, achalasia).
Use of antacids facilitates bacterial and fungal (candida) infections.

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