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GI Week 2 > ICL 4.3: Disorders in Emptying > Flashcards

ICL 4.3: Disorders in Emptying Flashcards

1
Q

what is nausea?

A

vague, unpleasant sensation of impending vomiting

nausea shares the same pathway of vomiting

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2
Q

what is retching?

A

muscular activity of the abdomen and thorax, often voluntary, leading to forced inspiration against a closed mouth and glottis without oral discharge of stomach contents

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3
Q

what is vomiting?

A

involuntary contractions of the abdominal, thoracic and GI (smooth) muscles leading to forceful expulsion of gastric contents through the mouth

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4
Q

what is regurgitation?

A

effortless return of esophageal or gastric contents into the mouth unassociated with nausea or involuntary muscle contractions

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5
Q

what is rumination?

A

food that is regurgitated in the postprandial period, re-chewed and then re-swallowed

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6
Q

where is the vomiting center located? what does it receive stimuli from?

A

the vomiting center is located in the lateral reticular formation in the Medulla Oblongata

it receives stimuli from:
1. high brain centers in response to pain, sights, smells, tests and emotional factors

  1. peripheral pathways that come from the GI system, viscera, heart, genitourinary system via the vagus and splanchnic nerves, sympathetic ganglia, and glossopharyngeal nerves

these are transmitted via the vagus and splenic nerves and sympathetic ganglia and glossopharyngeal nerves

  1. vestibular system via the vestibulo-cochlear nerves
  2. chemoreceptor trigger zone
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7
Q

what is the chemoreceptor trigger zone?

A

it’s located in Area Posterma in the floor of the 4th ventricle

it is sensitive to chemical stimulation (endogenous or exogenous agents) from cerebral spinal fluid and blood

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8
Q

what are the overall events in vomiting?

A

after the vomiting center receives stimuli it’ll initiate a cascade of events:

  1. suspension of intestinal slow wave activity
  2. retrograde contractions from ileum to stomach
  3. suspension of breathing; closed glottis to prevent aspiration
  4. relaxation of LES with contraction of abdominal muscles and diaphragm
  5. ejection of gastric contents through open UES
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9
Q

what are some of the symptoms prior to vomitng?

A
  1. profuse salivation
  2. sweating
  3. tachycardia
  4. nausea
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10
Q

what are the classes of causes of vomiting?

A
  1. mechanical
  2. inflammatory/infectious
  3. genitourinary
  4. CNS (intracranial pressure, vertigo )
  5. metabolic (diabetic ketoacidosis)
  6. other/atypical (toxins)
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11
Q

what are some common causes of nausea and vomiting?

A
  1. GI tract disorders: toxins, infections, obstruction, inflammation, motility disorders
  2. non-GI infections: liver, CNS, renal, pneumonia
  3. pregnancy
  4. visceral inflammation
  5. MI or myocardial ischemia
  6. CNS: migraine, neoplasm, bleed
  7. vestibular disorders
  8. metabolic/endocrine: DKA, uremia, adrenal insufficiency, hyper or hypothyroidism
  9. alcohol
  10. psychogenic
  11. radiation exposure
  12. medications
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12
Q

which medications can cause nausea and vomitng?

A
  1. cisplatin
  2. NSAIDs, opiates
  3. digoxin, quinidine
  4. erythromycin
  5. oral contraceptives
  6. metformin
  7. L-DOPA
  8. anticonvulsants like phenytoin and carbamazepine

10 . anti hypertensives

  1. theophylline
  2. anesthetic agents
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13
Q

what are the complications of vomiting?

A
  1. volume depletion
  2. metabolic: acid base abnormalities, electrolyte imbalances (hypokalemia), etc
  3. aspiration
  4. oropharyngeal (dental, sore throat)
  5. GI: Esophagitis, Mallory- Weiss tear, Boerhaaves Syndrome (includes muscle)
  6. nutritional deficiency
  7. renal: prerenal azotemia, ATN, hypokalemia
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14
Q

what are some acute causes of nausea and vomiting?

A

< 1 week

  1. cholecystitis
  2. gastroenteritis
  3. medication related effect
  4. pancreatitis
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15
Q

what are some chronic causes of nausea and vomiting?

A

1+ months

  1. partial obstruction
  2. motility disorder
  3. neurologic chronic condition
  4. functional causes
  5. pregnancy
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16
Q

what are causes of nausea and vomiting in the morning?

A
  1. alcohol ingestion
  2. increased intracranial pressure
  3. pregnancy
  4. uremia
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17
Q

what are some associated symptoms of nausea and vomiting?

A
  1. chest or abdominal pain
  2. fever
  3. myalgia
  4. diarrhea
  5. vertigo
  6. dizziness
  7. headache
  8. focal neurological symptoms
  9. jaundice
  10. weight loss
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18
Q

what is gastroparesis? what are the symptoms?

A

a delay in gastric emptying without any mechanical obstruction in the stomach

it affects up to 10 million individuals in the United States (3%); with 70% female; median age: 50 years

the cardinal symptoms are upper abdominal pain, postprandial fullness, bloating, early satiety nausea, and with more severe illness, vomiting

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19
Q

what is the pathogenesis of gastroparesis?

A

the motor function of he gut is controlled at 3 levels = autonomic vagal control, intrinsic, and extrinsic and disruption of any of these can lead to delayed gastric emptying

  1. altered gastric electrical activity
  2. decreased funds motor activity
  3. reduced astral motor activity
  4. hyperglycemia
  5. impaired antroduodenal coordiation
  6. dysfunction of inter digestive motor activity phase 3 = overnight retention of large indigestible food
  7. pyloric motility
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20
Q

what are the etiologies of gastroparesis?

A
  1. idiopathic
  2. diabetic
  3. upper GI surgery
  4. Parkinson’s
  5. collagen tissue disorder (scleroderma)
  6. intestinal pseudo-obstruction
  7. medications, eating disorders
21
Q

which drugs delay gastric emptying?

A
  1. opiates
  2. amylin analogs
  3. B-agonists
  4. anticholinergics
  5. tricyclic agents
  6. phenothiazines
  7. dopamine agonists
  8. PPIs
  9. dexgengluramine
  10. antihistamins
  11. cyclosporin A
  12. lithium
  13. tetrahydrocannabinol
  14. tobacco
22
Q

how do you diagnose gastroparesis?

A
  1. scintigraphic gastric emptying

most cost-effective, simple, widely available technique
Normal < 50% of solid residual gastric activity after 50-100 min
Less than 10% of solid gastric residual at 4 hours : most accurate (sensitivity-100%, specificity-70%)

  1. UGI series

to rule out mechanical obstruction; retention of barium without obstruction is highly suggestive

  1. esophagogastroduodenoscopy (EGD)

evaluation for structural pathologies; bezoar without obstruction is highly suggestive

23
Q

how do you treat gastroparesis?

A
  1. supportive measures and lifestyle modifications!!!
  2. hydration
  3. diet modification like low fat, low fiber diet with frequent small meals
  4. optimize glycemic control*
  5. improve gastric motor function
  6. treat nausea with antiemetics
  7. botulinum toxin pyloric injections
  8. surgery –> placement of gastric electrical stimulation system, pyloroplasty or gastric resection/total gastrectomy
  9. pro kinetic agents
24
Q

what are the prokinetic agents used to treat gastroparesis?

A
  1. motilides: erythromycin
  2. antidopaminergic agents: domperidone
  3. antidopaminergic/serotonergic agents: metoclopramide
  4. serotonergic agents: tegaserod, prucalopride
25
Q

what is cyclic vomiting syndrome?

A

recurrent and stereotypical episodes of severe nausea and vomiting seperated by symptom free intervals

gastric emptying is rapid or normal

associated with migraine headaches, and psychological disorders (depression/anxiety)

absence of compulsive hot water bathing! patients with cannabinoid hyperemesis syndrome patients DO have hot water shower compulsions!

responds to tricyclic antidepressant (TCA)

26
Q

what is cannabinoid hyperemesis syndrome?

A

cyclic vomiting syndrome

compulsive hot water bathing

responds poorly to TCAs; only thing that helps is stopping cannabis!

27
Q

what is surreptitious vomiting?

A

associated with unexplained weight loss, co-existent eating disorder or other psychological condition, and o-existent laxative and/or diuretic abuse

there are electrolyte and/or acid-base disturbances consistent with vomiting, including hypokalemic nephropathy

emetic complications (with denial of vomiting)

28
Q

what is infantile hypertrophic pyloric stenosis?

A

characterised by hypertrophy of the circular muscle layers of the pylorus resulting in gastic outlet obstruction

incidence: 1.5 to 4 per 1000 live births

male : female ratio = 4:1

29
Q

what is the etiology of infantile hypertrophic pyloric stenosis?

A
  1. genetic 11q14-22 and Xq23 (rarely autosomal dominant)
  2. familial
  3. ethnic: more commonly seen in caucasians
  4. erythromycin or azithromycin exposure
  5. transpyloric feeding of premature babies
30
Q

what conditions is infantile hypertrophic pyloric stenosis associated with?

A
  1. Turner syndrome
  2. TE fistula
  3. trisomy 18
  4. esophageal atresia
31
Q

what is the clinical presentation of infantile hypertrophic pyloric stenosis?

A

onset of symptoms at 2 to 8 weeks of age (commonly at around one month of age)

  1. projectile, forcible, frequent episodes of non- bilious coffee ground vomiting 30 to 60 minutes after feeding
  2. weight loss
  3. persistent hunger
  4. lethargy
  5. constipation

physical examination will show palpable,olive shaped, mobile, smooth, firm mass (1.5 to 2 cm) to right of epigastric area and visible gastric peristalsis from LUQ to epigastrium

32
Q

how do you diagnose infantile hypertrophic pyloric stenosis?

A
  1. abdominal X-ray –> upper abdominal gas bubble
  2. abdominal ultrasound** gold standard –> doughnut sign or cervical pyloric sign, pyloric muscle thickness 4+ mm
  3. barium test/fluoroscopy –> delayed gastric emptying, elongated and narrow pyloric canal = string sign
33
Q

how do you manage infantile hypertrophic pyloric stenosis?

A
  1. resuscitation with IV rehydration
  2. correct electrolyte abnormalities
  3. nasogastric tube drainage to prevent aspiration of vomited secretions
  4. surgery; pyloromyotomy
34
Q

how do you treat nausea and vomiting?

A
  1. identify and correct any complication
    e. g., electrolyte abnormalities, dehydration, bleeding, nutritional support
  2. identify and treat underlying cause
  3. provide temporary symptomatic relief
  4. use preventive measures when vomiting is likely to occur (e.g. steroids administration prior to chemotherapy)
35
Q

what is the vomiting pathway? which drugs act at which parts?

A
  1. stomach, small intestine –> chemoreceptor trigger zone –> vomiting center in the medulla –> vomiting reflex

5-HT3 RAs and cannabinoids block the stomach/small intestine –> chemoreceptor trigger zone

5HT3 RAs, H1 RAs, muscarinic RAs, D2 RAs and NK1 RAs block trigger zone –> medulla

  1. higher cortical centers –> vomiting center in the medulla –> vomiting reflex

H1 RAs, GAVA, and cannabinoids block the higher cortical centers

  1. labyrinths –> vomiting center in the medulla –> vomiting reflex

muscarinic RAs block labyrinths

36
Q

what are the classes of antiemetics?

A
  1. antihistaminic
    ex. meclisine, diphenhydramine; good for vestibular disorders
  2. antidopaminergic
    ex. chlorpromazine, prochlorpermine, metoclopromide, domperdione; good for GI disorders
  3. serotonin antagonists
    ex. granisetron, ondansetron, palonosetrone; good for chemo induced nausea
  4. neurokinin-1 antagonists
    ex. aprepitant; good for chemo induced nausea
  5. anticholinergic
    ex. scopolamine; good for vestibular and GI disorders
  6. corticosteroids
    ex. dexamethasone
  7. cannabinoids
    ex. nabilone, dronabinol
37
Q

what is the MOA of phenothiazines?

A

dopmine antagonistic effects in CTZ

side effects = restlessness and dystonia

ex. prochlorperazine, chlorpromazine

38
Q

what is the use and side effects of serotonin antagonists?

A

works well for chemo induced nausea and vomiting

side effects = headaches and constipation

39
Q

what is metoclopramide?

A

prokinetic agent used for nausea

central and peripheral dopaminergic and serotonergic antagonist that increases gastric emptynig

side effects:
1. extrapyramidal signs (parkinson like syndrome, tardive dyskinesia)

  1. restlessness,
  2. hyperprolactinemia
  3. boxed warning for chronic use
40
Q

what is domperidone?

A

prokinetic agent used for nausea

peripheral dopaminergic antagonists that improves gastric emptying

side effect = QT prolongation

41
Q

what is erythromycin

A

prokinetic agent

motilin receptor agonists

no antiemetic effect!!!!!

stimulates astral contraction and MMC

side effect:
1. GI toxicity

  1. ototoxicity
  2. QT prolongation
42
Q

what are the uses and side effects of antihistamines?

A

for nausea and vomiting due to vestibular causes, or motion sickness

side effects may include : drowsiness, dry mouth

ex. meclisine, diphenhydramine

43
Q

what are the uses and side effects of anticholinergics?

A

possible adjunct for cytotoxic chemotherapy, prophylaxis and treatment of motion sickness

side effects: drowsiness, dry mouth, vision disturbances

ex. scopolamine

44
Q

what is a hiatal hernia?

A

a condition involving herniation of the contents of the abdominal cavity, most commonly the stomach, through the diaphragm into the mediastinum

the esophagus enters the abdomen through the diaphragmatic hiatus, anchored at the level of the esophagogastric junction by the phrenoesophageal membrane.

the right crus and lower esophageal sphincter together form the GE junction which acts as a barrier against the reflux of gastric content into the esophagus.

the hiatus is vulnerable to visceral herniation because it is directly subject to pressure stress between the abdomen and the chest

45
Q

what are the risk factors for hiatal hernias?

A
  1. age
  2. increased intra-abdominal pressure
  3. obesity
  4. pregnancy
  5. lifting heavy objects,
  6. history of gastroesophageal surgery
  7. thoracoabdominal trauma
  8. congenital defects
  9. skeletal deformities
46
Q

what is the clinical presentation of hiatal hernias?

A

the majority are asymptomatic!

  1. GERD = heartburn, regurgitation, dysphagia
  2. epigastric or substernal pain
  3. postprandial fullness
  4. nausea & retching
47
Q

what are the complications of hiatal hernias?

A
  1. gastric volvulus with or without strangulation
  2. complicated GERD
  3. chronic blood loss from gastric ulceration, gastritis, or erosions (Cameron lesions)
  4. respiratory complications from a large hernia
48
Q

how do you diagnose hiatal hernias?

A
  1. barium swallow
  2. upper endoscopy
  3. esophageal manometry
49
Q

how do you manage hiatal hernias?

A

surgical repair of an isolated, asymptomatic type I hiatal hernia is not indicated.

symptomatic sliding hiatus hernia consists of management of GERD

surgical treatment might be considered with persistent regurgitation despite medical treatment (chronic cough refractory to PPI, intolerance to PPIs, or refractory esophagitis).

the standard procedure is currently laparoscopic fundoplication

mobilizing the lower esophagus, reduce the hiatus hernia, and wrap the gastric fundus around the esophagus

GI Week 2 (10 decks)

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