Gi Exam 2: Motility Disorders

Front 1

explain the functional esophageal anatomy

Back 1

esophagus is ~25cm long muscular tube, has sphincter at the top and the bottom

Front 2

sphincters prevent __ of __ and __ into the esophagus

Back 2

prevent INFLUX of AIR and REFLUX (of gastric contents) into the esophagus

Front 3

describe normal esophageal peristalsis

Back 3

quick upstroke and downstroke of muscular contraction during a swallow. as soon as swallow begins, the LES relaxes and contracts after swallow is completed

Front 4

describe the pathophysiology of achalasia

Back 4

lack of peristalsis in the esophageal body, non-relaxation of LES. the LES basal pressure can be normal, sometimes high in achalasia

Front 5

do motility disorders lead to solid dysphagia only or solid and liquid dysphagia?

Back 5

solid and liquid! (remember, strictures or obstructions lead to solid dysphagia)

Front 6

why does achalasia occur?

Back 6

inflammatory infiltrate in myenteric plexus --> ganglionic drop-out (may be result of virus, may be idiopathic)

Front 7

in south america, ___ is the primary cause of ___.

Back 7

CHAGAS DISEASE (a parasite infection) is the primary cause of ACHALASIA

Front 8

presentation of achalasia (4 sx)

Back 8

dysphagia, chest pain, heartburn, regurgitation. may have compensatory mechanisms (jumping etc.) to help get food down.

Front 9

3 complications of achalasia

Back 9

malnutrition, pulmonary complications (due to aspiratoin), squamous cell carcinoma (due to stasis)

Front 10

achalasia barium swallow

Back 10

dilated esophagus, bird beak (smooth symmetric narrowing at distal esophagus), ?debris

Front 11

in achlasia, diagnostic endoscopy is primarily done to ___.

Back 11

RULE OUT strictures and masses

Front 12

what is the tx of achalasia for patients that aren't good candidates for surgery?

Back 12

botulinum toxin injection (effect ~6 mo.s). blocks presynaptic ACh release

Front 13

describe pneumatic dilation. what disease is it used for? what is the major complication it's associated w/?

Back 13

used to treat achalasia, put a balloon across GE junction and rapidly inflates balloon up to 3-4cm --> ruptures the muscle. major complication is PERFORATION (also GERD).

Front 14

what is the tx of choice for achalasia?

Back 14

esophageal myotomy. slice through LES and some of esophagus and wrap fundus of stomach around it. only relieves obstruction. (this DOES NOT improve peristalsis)

Front 15

describe esophageal spasm.

Back 15

repetitive, simultaneous, abnormally long contractions of esophagus in response to swallow

Front 16

esophageal spasm etiology and presentation

Back 16

etiology: unclear. presentation: chest pain, dysphagia

Front 17

diffuse esophageal spasm on barium swallow

Back 17

corkscrew esophagus (b/c contractions are not coordinated)

Front 18

how does diffuse esophageal spasm look on manometry?

Back 18

repetitive high pressure spikes. bright red/purple color throughout esophagus, slight relaxation of LES.

Front 19

diffuse esophageal spasm therapy

Back 19

smooth muscle antagonists (calcium channel blockers, nitrates); occasionally will need surgery (long myotomy); not good research on best treatment of diffuse esophageal spasm

Front 20

describe ineffective esophageal motility

Back 20

characterized by weakened peristalsis, often seen in association w/reflux disease. presentation is dysphagia. **peristalsis is retained, but amplitude is reduced.

Front 21

___ is esophageal asystole, ___ is esophageal tachycardia, and ___ is esophageal CHF

Back 21

achlasia is asystole, diffuse esophageal spasm is tachycardia, ineffective esophageal motility is CHF

Front 22

describe peristalsis in ineffective esophageal motility

Back 22

weak, low amplitude contractions, some of which are not transmitted, following swallow

Front 23

CREST syndrome

Back 23

calcinosis + raynaud's syndrome + esophageal dismotility + sclerodactyly + telangiectasias (shows up w/scleroderma)

Front 24

sclerodoerma etiology and pathophysiology

Back 24

autoimmune. pathophys: diffuse fibrosis, inflammation, and vasculopathy. affects skin and internal organs

Front 25

name 6 skin findings associated w/systemic sclerosis

Back 25

mouth doesn't open wide b/c of tightened skin, beaking of nose, sclerodactyly (tightening and thickening of skin on fingers), calcinosis, raynaud's phenomenon, digital ulceration

Front 26

what organs are affected by scleroderma?

Back 26

GI tract (esophagus), skin, kidneys, lungs

Front 27

how does scleroderma affect the esophagus?

Back 27

collagen replaces muscle --> GI myopathy throught the tract. in the esophagus, the LES is destroyed (REFLUX) and peristalsis is decreased (DYSPHAGIA) --> refluxate isn't cleared --> severe esophagitis

Front 28

how does scleroderma affect the stomach?

Back 28

collaen replaces muscle --> GI myopathy --> gastric stasis (gastroparesis) --> NAUSEA and VOMITING

Front 29

how does scleroderma affect the small intestine?

Back 29

collagen replaces muscle --> GI myopathy --> impaired motility --> BLOATING, NAUSEA, can lead to bacterial overgrowth (diarrhea, fat malabsorption)

Front 30

how does scleroderma affect the large intestine?

Back 30

collagen replaces muscle --> GI myopathy --> impaired motility --> CONSTIPATION

Front 31

does scleroderma cause constipation or diarrhea?

Back 31

can cause both! constipation b/c of colon dysmotility, diarrhea b/c of sml intestine dysmotility

Front 32

true or false: scleroderma causes a neuropathy

Back 32

false. scleroderma is a MYOPATHY. acholasia is a NEUROPATHY.

Front 33

vomiting is a ___ ___.

Back 33

COORDINATED EVENT. comes from the CNS (vomiting center)

Front 34

list 5 processes involved in vomiting

Back 34

1. higher center and vomiting center CNS control. 2. antiperistalsis (reverse peristalsis) 3. stomach squeezing 4. contraction of diaphragm and abdominal muscles 5. LES relaxation

Front 35

name 5 stimuli that lead to vomiting

Back 35

vestibular stimuli, sensory input (bad smell), emetics (blood-borne), local irritants, memory

Front 36

name the top 5 things on your differential Dx for acute nausea and vomiting

Back 36

infection, toxin, obstruction, trauma, pregnancy

Front 37

name the top 6 things on your differential dx for chronic nausea and vomiting

Back 37

motility d/o (GI), toxic (meds), endocrine, other chronic GI disorders, obstruction, increased intracranial pressure (mass lesion in the brain, e.g.)

Front 38

during normal gastric emptying, the ___ relaxes to accommodate a meal, and the ___ grinds and sieves solids and pumps ____ through the ___, which has phasic and tonic contractions.

Back 38

fundus relaxes to accommodate a meal, the antrum grinds and sieves solids, the antrum pumps chyme through pylorus, which has phasic and tonic contractions. (all this receives feedback from nutrients in the small intestine)

Front 39

what is gastroparesis?

Back 39

lack of gastric motility or emptying in the absence of obstruction

Front 40

4 etiologies of gastroparesis

Back 40

DIABETES, scleroderma, drugs (e.g., opioids), idiopathic

Front 41

physical findings of gastroparesis (specific)

Back 41

hypovolemia, succussion splash

Front 42

symptoms of gastroparesis

Back 42

nausea/vomiting, bloating, epigastric pain, wt loss

Front 43

dx of gastroparesis

Back 43

upper endoscopy to r/o physical obstruction + gastric emptying study

Front 44

management of gastroparesis

Back 44

dietary changes (and control the DM!), prokinetic agents (e.g., metoclopramide), surgery, neurostimulators?

Front 45

where does bowel obstruction occur? how does this affect the differential dx?

Back 45

may occur anywhere along the GI tract, presentation is based on site (abd pain, n/v, bloating/distension, constipation/obstipation), and differential varies based on the site

Front 46

first you make the diagnosis of bowel obstruction. then, what's your differential for INTRINSIC bowel obstruction?

Back 46

neoplasms, ulcers, stenosis, foreign body

Front 47

first you make the diagnosis of bowel obstruction. then, what's your differential for EXTRINSIC bowel obstruction?

Back 47

adhesions (surgeons), pancreatitis, neoplasms, endometriosis

Front 48

first you make the diagnosis of bowel obstruction. then, what's your differential for H - I - V bowel obstruction?

Back 48

hernias (internal), intussusception, volvulus

Front 49

__ ___ can present just like ___

Back 49

motility disorders can present just like obstruction!

Front 50

describe radiographical findings of obstruction (gastric outlet, small bowel, large bowel)

Back 50

all present w/DILATION. gastric outlet shows stomach dilated, sml bowel looks like coins, large bowel is big air filling colon

Front 51

what is a volvulus? where are the 2 most common ones?

Back 51

twist of hollow organ (can twist b/c of mesentery not holding it firmly in place). cecal volvulus and sigmoid volvulus are most common.

Front 52

coffee bean pattern is a common __ finding of ___

Back 52

radiologic finding of volvulus. the coffee bean "points" to the region of the twist itself.

Front 53

what is intussusception?

Back 53

bowel telescopes along itself. in pediatrics, this can happen w/infections (?viral, rotavirus vaccine)

Front 54

in adults with intussusception, you must ___. (what is at the top of your DDx?)

Back 54

IDENTIFY THE LEAD POINT. malignancy is at the top of your ddx.

Front 55

radiographical findings of intussusception?

Back 55

x-section looks like a target (multiple layers of hypo-/hyper-dense areas), circumferential circles on ultrasound

Front 56

how do you manage bowel obstruction?

Back 56

SITE DEPENDENT. most require surgery. decompression (NG tube) + assessment of etiology --> ultimate tx based on underlying etiology

Front 57

intrinsic bowel obstructions are __, extrinsic bowel obstructions are ___.

Back 57

intrinsic bowel obstructions are luminal, extrinsic bowel obstructions are peritoneal.