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Gastroparesis Flashcards

1
Q

What is gastroparesis?

A

SYMPTOMS consistent with delayed gastric emptying

WITHOUT mechanical obstruction

AND delay in 4 hr solid phase gastric

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2
Q

Gastroparesis is usually caused by:

A

50% idiopathic!! Mostly women
Neuropathy.
Injury to the ENS is common
Vagal injury is not the cause in all patients

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3
Q

What are the Sx of gastroparesis?

A 
N/V
Early satiety
Epigastric pain
Anorexia and weight loss
GERD
Bloating
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4
Q

What are some causes of gastroparesis?

A 
Diabetes
Surgery
Ischemia
Neurologic
Inflamatory
Meds
Transplant
Cirrhosis
Paraneoplastic
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5
Q

Describe the five components of the pathophys of gastroparesis

A
  1. Fundal hypomotility
  2. Antral hypomotility
  3. Antropyloroduodenal spasm
  4. Gastric pacemaker dysrhythmias
  5. excessive inhibitory feedback w/ NO or VIP
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6
Q

What’s on your differential for gastroparesis?

A

Functional dyspepsia
Mechanical obstruction
rumination
Medication

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7
Q

What are the complications of gastroparesis?

A
  1. bezoar
  2. GERD
  3. Cholecystectomy
  4. Mallory-weiss tear
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8
Q

What is the best test for gastroparesis?

A

4 hour solid phase gastric emptying scan

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9
Q

How do we treat gastroparesis?

A
  1. Diet: Small, low fat/fiber meals with liquids
  2. Prokinetics (metoclopramid and erythromycin
  3. Antiemetics
  4. gastric stimulation
  5. Surgery
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10
Q

How does metoclopramide work?

A

Increases ACh release

Inhibits dopamine receptors everywhere

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11
Q

What are the side effects of metoclopramide?

A

Tardive dyskinesia

Also acute dystonic reaction, parkinsonism

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12
Q

How does erythromycin work?

A

Induces Phase III of the MMC

–>more antral contractions

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13
Q

What are some challenges in treating gastroparesis?

A
  1. Symptoms do not correlate with rate of gastric emptying
  2. Treat predominant synptom
  3. Avoid surgery
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14
Q

What are the diagnostic criteria for functional dyspepsia?

A

Rome III: 1+ of the following

  1. Bloating after meals
  2. Early satiety
  3. Epigastric pain (most common)
  4. Epigastric burning

ALSO, no evidence of structural disease and 3 months of Sx PLUS onset 6 mos before diagnosis

Weight loss is also common

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15
Q

What are common causes of functional dyspepsia?

A
  1. Genetics
  2. Post-infectious
  3. inflammatory state
  4. Meds
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16
Q

What studies might be helpful for functional dyspepsia?

A

Upper endoscopy
CBC, LFT< ESR
–If vomiting, consider gastric emptying scan

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17
Q

What is highest on your differential for functional dyspepsia?

A

Gastroparesis

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18
Q

Treating FD is difficult–there’s no one medication that works! What are available options?

A
  1. Dietary/lifestyle changes
  2. H pylori eradication
  3. Antisecretory therapy (lowers acid secretion)
  4. Prokinetics
  5. Tricyclic antidepressants (SNRIs not effective)
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19
Q

What is the most common functional gastrointestinal disorder?

A

The most common functional gastrointestinal disorder–10-12%. Abdominal PAIN + discomfort and a change in bowel function

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20
Q

What are the diagnostic criteria for IBS?

A

Rome III:

  1. Recurrent abdominal pain or discomfort WITH 2+ of the following:
    - Improves with defecation
    - change in stool frequency
    - change in stool form

At least 3 months with Sx and 6 mos after onset. DEFINED by Sx with normal blood work, imaging, and endoscopy

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21
Q

What are the three types of IBS?

A
  1. constipation
  2. diarrhea
  3. alternating
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22
Q

Describe the pathophysiology of IBS

A

A bunch of genetic/environmental/other factors affect serotonin, CRF, and adenosine levels in brain and bowel causing a change in motility, and visceral hypersensitivity

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23
Q

What are the four main symptoms of IBS?

A
  1. Abdominal pain/discomfort
  2. Bloating
  3. Constipation
  4. Diarrhea
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24
Q

What are some red flags when evaluating a pt with suspected IBS that would lead you down another path?

A
  1. weight loss
  2. > 50 yrs
  3. Anemia
  4. High ESR or WBC or TSH
  5. Rectal bleeding
  6. Arthritis/rashes
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25
Q

What is the purpose of doing a colonoscopy in IBS?

A

Not that useful…except for identifying more patients with microscopic colitis in pts > 45 years

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26
Q

How do you treat IBS?

A

Treat the symptom:
1. Pain=Antidepressants
2. Bloating: Serotonin agonist, or dietary
3. Constipation: Fiber, Mom/PEG
4. Diarrhea: Loperamide, Serotonin agonist
All can be treated with serotonin agonists/antagonists.

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27
Q

What is the IBS diet?

A

Low carbs, fructose, gluten, Fermentable Oligo, Di, Mono, polysaccharides and Polyols(FODMAP)

  • No fruits
  • No wheat/rye
  • No artificial sweeteners w/ sorbital
  • No raffinose (lentils/cabbage, brussels, asparagus)
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28
Q

What CAN you eat on IBS?

A

lean protein

  • gluten free
  • rice/corn/oat
  • Select fruit/veg
  • snow peas, bok choy, mandarin oranges
29
Q

What other therapies (microbiome related) that can be used in IBS?

A

Probiotics (bifidobacteria)

Antibiotics (Rifaximin

30
Q

What is the only drug that has been approved to treat IBS-D?

A

Alosetron. It’s a serotonin (5hT-3) receptor antagonist

31
Q

What anti-osmotic agent is useful for IBS?

A

PEG

32
Q

What drug is approved for IBS-C?

A

Lubiprostone, a type 2 chloride channel activator

-Increases choloride in lumen, Na follows to balance charge, and H2O follows

33
Q

What are the enteric nervous system neurons derived from? What does it receive input from?

A

Neural crest cells

–Input from CNS and ANS, but is SELF functioning!

34
Q

What are the two components of the enteric plexus?

A

submucosal and myenteric plexi

35
Q

Which two layers does the submucosal plexus lie between? Which sections of the GI tract does it populate?

A

The inner circular muscle layer and mucosa. Found only in the small and large bowel

36
Q

Between which two layers does the myenteric plexus lie btw? Which sections of the tract does it populate?

A

Between muscular inner circular and outer longitudinal layers. Found along the whole GI tract.

37
Q

What does the submucosal plexus innervate?

A
  1. Secretory cells
  2. Endocrine cells
  3. Blood vessels
38
Q

What does the myenteric plexus innervate?

A
  1. SECRETOmotor innervation
39
Q

What are the major excitatory neurotransmitters in the GI tract?

A

Ach, substance P, and tachykinins

40
Q

What are the major inhibitory neurotransmitters in the GI tract?

A

Nitric oxide

VIP

41
Q

What is the role of serotonin in the GI tract?

A

Found in interneurons for motor, sensory, and secretory fxn

42
Q

What are IPANs?

A

Intrinsic primary afferent neurons. They are the primary neurons carrying sensory signals and are embedded in the mucosa.

In contrast, extrinsic afferent neurons have cell bodies in DRGs

43
Q

What do interneurons do?

A

Helps with crosstalk btw sensory and motor neurons (myenteric plexus) to cause peristalsis.

44
Q

The main fxn of the vagus nerve in the GI is:

A

SENSORY afferent!

45
Q

Describe the physiology of peristalsis

A

IPAN–>Myenteric plexus–>interneuron in myenteric plexus–>efferent motor neuron in myenteric plexus

46
Q

What are the pacemaker cells of the gut?

A

Interstitial cells of cajal. “Pace” of the stomach is slower than the small intestine

47
Q

What is the main fxn of the fundus?

A

Accommodating the food. High tone and low peristalsis

48
Q

What is the main fxn of the antrum?

A

Grinding food. Low tone and high peristaltic activity

49
Q

What nerve helps expand the fundus and initiate the grinding action of the antrum?

A

The vagus

50
Q

What will a normal/abnormal EGG look like (Electrogastrography)?

A

Normal: coordinated movement
Abnormal: Not coordinated

51
Q

What is gastric motility in the fed state?

A

Persistent, irregular contractile activity

52
Q

What is gastric motility in the fasting state?

A

MMC:
Phase I: quiescence
Phase II: irregular phasic activity (antrum)
Phase III: short period of intense contraction (smal bowel)

53
Q

What is the pathogenesis of nausea/vomiting?

A

Vagal/sympathetic afferents from all over–>stimulate vomiting center in medulla

OR: Chemoreceptor in area postrema of 4th ventrical outside BBB–>vomiting center

OR: afferents from CNS–>stimulate vomiting center

54
Q

What is the most common acute cause of nausea and vomiting?

A

INFECTIONs

55
Q

What are common causes of chronic N/V?

A

gastroparesis
Intestinal pseudo-obstruction
Psychogenic vomiting

56
Q

What is the one symptom REQUIRED for gastroparesis?

A

Vomiting

57
Q

What is the “braking mechanism” for the small bowel?

A

ileocecal valve

58
Q

What stimulates the GI externally?

A

Parasympathetic innervation

59
Q

What inhibits the GI internally?

A

Sympathetics

60
Q

Which syndromes cause disorders in small bowel dysmotility?

A
  1. Scleroderma
  2. Hollow Visceral myopathy
  3. Intestinal pseudo-obstruction
  4. Irritable bowel syndrome
61
Q

What happens in scleroderma?

A

Aperistalsis from loss of GI smooth muscle

  • ->Esophagus most common, then small intestine/anorectal.
  • ->gastric motility is preserved, with its 3 layers of muscle
62
Q

What is the fxn of the colon?

A

Absorption
Formation of residue (poo poo)
storage
Transport

63
Q

What are the three types of normal colonic motor patterns?

A
  1. Segmenting contractions (for mixing)

2. Propagating contractions (Low amplitude for short distance, high amplitude for long distances post meal)

64
Q

What is Hirschsprung’s disease?

A

Failure of neural crest cells to move to the colon. Aganglionosis.

Sx: failure to thrive, distention, bloating, constipation. Pt won’t poop, with colonic dilation above affected segment

65
Q

How do you diagnose hirschsprung’s?

A

anorectal manometry or biopsy

66
Q

How do you tx hirschsprung’s?

A

surgery

67
Q

What is anorectal manometry?

A

Put a balloon in rectum. Normally will cause RAIR (recto-anal inhibitory reflex) causing relaxation of the internal sphincter. The external sphincter is consciously controlled

68
Q

What is colonic inertia?

A

Happens in young women, with infrequent stools (every 1-4 weeks)

Caused by loss if ICC cells

GI (27 decks)

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