Ray - Gastroparesis Flashcards
1
Q
How does the gastric pacemaker work? Measurement?
A
- Slow waves originate in pacemaker region at juncture of fundus and corpus on greater curvature
- Slow waves propagate circumferentially, migrate distally to pylorus at a rate of 3 cycles/min (cpm), or about 1 every 20 seconds
- The fundus does NOT have slow wave activity
- NOTE: summed gastric myoelectrical activity from electrodes on abdominal surface in epigastrium is electrogastrogram (EGG); normal rhythm is 3 cpm
2
Q
What is the role of the stomach in food processing?
A
- No absorptive potential, but rather breaking things down, and sending to small bowel for absorption
- Food into fundus, which relaxes, INC volume, then waves begin, beat food into smaller particles that move toward antrum and pylorus, meeting resistance
- Chyme is the result, which enters small intestine: if a large particle makes it through, small intestine may have trouble digesting it, and you may have diarrhea
3
Q
How does “normal” gastric emptying work?
A
- To accommodate vol of food w/o INC intragastric pressure, fundic smooth muscle relaxes, receiving ingested foods (receptive relaxation)
- Fundus contracts to empty ingested food in corpus and antrum for trituration and emptying
- Recurrent corpus-antral peristaltic waves mill solids into chyme, 1-2mm solid particles suspended in gastric juice
- Antral peristaltic waves empty 2-4mL of chyme into pylorus and duodenal bulb at slow wave frequency
- Antropyloroduodenal coordination indicates efficient emptying of chyme through pylorus, which modulates flow of chyme by varying sphincter resistance
- Contractions in duodenum also provide resistance to emptying
4
Q
What is gastric accomodation?
A
- Fundus and proximal stomach expand during meal
- Measured with a barostat balloon in this case, and INC from 200 mL to 450 mL in 20 min after the meal is ingested
- As the meal is emptied, volume in stomach slowly DEC over two-hour postprandial period
- Relaxation of prox stomach and accommodation of meal volume reflect vagal-mediated receptive relaxation
5
Q
What does this image show you?
A
- Gastric emptying study: takes 4 hrs for food to leave the stomach (almost no food left at this pt: about 5%)
- Persistence of portions of the meal in fundus at 120 min post-ingestion: meal slowly redistributed from fundus to antrum for trituration and emptying
- Note on the attached graph that only about 15% of food is emptied in first 45 minutes, the lag phase of gastric emptying
1. About 50% emptied at 90 minutes
6
Q
How is solid vs. liquid mvmt through the stomach different?
A
- Liquid moves through the stomach much more quickly
- 80% gone after 60 minutes vs. about 50% of solid meal
7
Q
What do you see here?
A
- US images of accomodation after eating soup
- Antrum, corpus, and fundus distend, indicating the marked relaxation of the smooth muscle required to accommodate this volume of liquid
8
Q
What is gastroparesis? Cardinal symptoms?
A
- Syndrome of objectively delayed gastric emptying, in the absence of mechanical obstruction
-
Cardinal symptoms: N/V, early satiety, bloating, abdominal pain
1. Can devo weight loss over prolonged period
9
Q
What is the epi of gastroparesis?
A
- 9.6-38 per 100,000 (4x as common in women)
- Most common in young people -> mean age of onset 34-y/o
- 80% of cases women
10
Q
What are some of the causes of gastroparesis?
A
- # of different entities can lead to common pathway of gastroparesis: NOT just one physiological disorder
- Could be CNS, spinal cord injury, idiopathic, diabetic neuropathy, infiltrative processes, etc. -> can all lead to similar symptoms and same diagnosis
- NOTE: he said not to worry too much about these
11
Q
Describe the spectrum of gastric NM disorders.
A
- Abnormal fundic relaxation and emptying: early satiety
- Gastric dysrhythmias and antral hypomotility: pace-maker abnormalities (brady - tachy)
- Pyloric sphincter dysfunction (pylorospasm): can inject Botox into the pylorus, but unclear whether this is very effective
- Duodenal dysfunction, antroduodenal dyscoordination, vagal neurohypersensitivity
12
Q
What is the difference between these two images? Why is this important?
A
- LEFT: EGG from pt w/gastroparesis due to mech obstruction at pylorus 2o to chronic PUD -> note persistent, high-amplitude 3cpm waves
- RIGHT: EGG in pt w/idiopathic gastroparesis -> note the 7-8cpm tachygastria, suggesting electrical and contractile abnormalities of the stomach
- Can’t dx gastroparesis w/o verifying there is no blockage, which can produce same symptoms (RCA tracing in these images not necessary to make dx)
13
Q
What is the etiology of gastroparesis?
A
-
Most common: idiopathic (up to 50% of all cases)
1. Diabetic
2. Post-surgical -
Others: post-infectious -> viral enteritis with N/V, but then have persistent symptoms after recovery
1. Neurologic disease
2. Autoimmune
14
Q
What meds can delay gastric emptying?
A
- Narcotics
- Clonidine
- Calcium channel blockers
- Tricyclic antidepressants
- Others
15
Q
What is the pathogenesis of diabetic gastroparesis? T1D vs. T2D? Tx?
A
-
Pathogenesis: only partially understood, but more common with long hx of disease, and poor control
1. Partially related to neuropathy
2. Hyperglycemia itself can cause delayed emptying (even in the healthy individual) -
Type I DM: usually only develops after 10 years
1. 27-58% of pts will develop gastroparesis - Type II DM: develops in up to 30% of Type II DM
- Good control of blood sugar is first-line therapy for these folks
16
Q
Which one of these graphs is from a hyperglycemic pt? How do you know?
A
- BOTTOM: tachygastria -> disruption of propagation, and onset 5-6-cpm tachygastria in distal lead during hyperglycemia (blood glucose level of 240 mg/dL)
1. INC rate of electrical pacemaker activity in the stomach, defined as >4cpm for at least 1 minute
2. Can induce tachygastria with hyperglycemia - TOP: 3cpm slow waves in prox, middle, and distal leads propagated in aborad direction (indicated by dotted lines)
18
Q
What are some of the causes of post-surgical gastroparesis?
A
- Previous gastric or thoracic surgery -> damage to Vagal nerves
- Common surgeries:
1. Billroth II: for refractory PUD and gastric adenocarcinoma -> don’t do much anti-ulcer surgery anymore due to efficacy of PPI’s
2. Fundoplication: GERD surgery, repair of hiatal hernia -> upper portion of stomach wrapped around lower esophagus
20
Q
How do you evaluate gastroparesis?
A
- Start with H + P
- Exclude mechanical obstruction (ex: malignancy, ulcer near pylorus):
1. Upper endoscopy
2. Consider CT or barium studies: dilated stomach due to chronic obstruction attached
21
Q
What’s up with this gastric outlet?
A
- It’s obstructed!
- It should look more like the attached photo
22
Q
What is one of the ways to relieve gastric obstruction by an un-resectable tumor?
A
- Put in a stent -> palliative procedure
- Resecting the tumor would be the primary tx, if possible
23
Q
What is the best test for diagnosing gastroparesis? How does it work? Dx?
A
- Gastric emptying study: for solid foods
- Stop meds that affect gastric emptying for 48 hours, including narcotics and motility agents
- Blood glucose needs to be < 275
- Pts eat a low fat, egg white meal labeled with 99mT-sulfur colloid w/imaging at 0, 2, & 4 hours afterward
1. Diagnostic GOLD STANDARD the 4-hr result: >10% = gastroparesis
2. Gastroparesis if >60% left at 2 hrs - May be over-diagnosis due to failure to continue this test long enough: probably okay if >60% at 2 hours, and <10% at 4 hours
25
Q
How are the symptoms of functinal dyspepsia and gastroparesis (dis)similar?
A
- Vomiting the main difference: more in gastroparesis
- A lot of overlap, and similar symptoms -> there may be some over-diagnosis of gastroparesis
26
Q
How are functional dyspepsia and gastroparesis different?
A
- Symptoms similar, but degree of gastric emptying may be dissimilar
- May dx someone with mild delay in emptying as functional dyspepsia, but if it is severe, probably gastroparesis
- Gastroparesis pts can also have rapid emptying on gastric emptying studies sometimes
- Basically, there is a lot of confusing overlap here…
29
Q
Metoclopramide
A
- D2 (dopamine) antagonist that enhances gastric antral contractions; first-line therapy
- FDA-approved for up to 12 weeks use (4x/day)
- Side effects limit use in up to 30% of patients
1. Drowsiness, fatigue, agitation
2. Hyperprolactinemia: impotence, galactorrhea, amenorrhea -> reversible w/discontinuing drug - Tardive Dyskinesia BBW: reason for the 12-wk limit
1. Irreversible, catastrophic side-effect
2. 1-10% of pts when taken >3 mos
2. Repetitive, involuntary, purposeless mvmts: grimacing, lip smacking, tongue mvmts, blinking
