GI: Esophagus Flashcards

(84 cards)

1
Q

incidence of cleft lip/ palate

A

1:1,000 births

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2
Q

Female or male MC for cleft lip

A

F>M

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3
Q

Female or male MC for cleft palate

A

M>F

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4
Q

ethnic groups with highest rate of CL or CP

A

asians

native americans

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5
Q

difference between syndromic and nonsyndromic CL or CP

A

syndromic: occurs as part of a chromosomal, mendelian or teratogenic syndrome
nonsyndromic: when CL CP occurs alone

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6
Q

epigenetic causes of CLP (3)

A

EPIGENETIC=non genetic causes

  • maternal smoking
  • maternal ETOH, steroid or statin use
  • maternal folate deficiency
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7
Q

define cleft lip

*when does it start

A

incomplete fusion of the nasomedial or intermaxillary process
*starts fourth week gestation

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8
Q

what other structures of the face can a cleft lip affect

A

not only the lip but also:

  • external nose
  • nasal cartilages
  • nasal septum
  • alveolar processes
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9
Q

cleft lip unilateral or bilateral?

A

MC one nostril but can be bilateral

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10
Q

cleft palate:

-define

A

often associated with cleft lip but can occur alone

  • fissure involves the uvula and soft palate
  • can extend forward into the nostril and involve hard palate and maxillary alveolar rdige
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11
Q

CMs for CL and CP

A
  • feeding difficulties

* obvious malformation

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12
Q

Evaluation and tx for cleft lip/palate

A

US and postnatal imaging
surgical correction
speech training
prosthodontist and orthodontit follow up

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13
Q

increase risk of ____ with CLP

A

middle ear infections

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14
Q

what is the MC congenital esophageal anomaly

A

Esophageal atrisia

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15
Q

how does the esophagus usually end?

A

in a blind pouch

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16
Q

what can esophageal atresia be accompanied with?

A

tracheoesophageal fistual

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17
Q

esophageal atresia MC associated with?

A

other congenital disorders

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18
Q

Infantile hypertrophic pyloric stenosis

  • define
  • common cause of?
  • incre freq in who?
  • why is there stenosis
A

acquired (or congenital**)

  • narrowing and distal obstruction of the pylorus
  • common cause of postprandial vomiting
  • increased frequency in first born males
  • individual muscle fibers thicken– entire pyloric sphincter becomes enlarged and inflexible*
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19
Q

postprandial vomiting want to think of?

A

infantile hypertrophic pyloric stenosis

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20
Q

why is the vomit with pyloric stenosis nonbilious?

A

because the food is not making it to the duodenum

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21
Q

what is pyloric stenosis also associated with

A

other developmental abnormalities

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22
Q

is infantile GERD pathologic in a normal healthy baby?

A

no

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23
Q

when does infantile GERD become pathologic

A

when reflux causes troublesome symptoms or complications

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24
Q

causes of infantile GERD

A
  • transient lower esophageal sphincter relaxations

- inadequate adaption of spichter tone to changes in abdominal pressure

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25
define reflux
passage of gastric content into the esophagus
26
define dysphagia
difficulty swallowing
27
list two general causes of dysphagia
mechanical (structural) obstruction OR Functional (motility) disorders
28
functional dysphagia | causes?
``` PROPULSION: caused by NEURONAL or muscular disorders -interfere with voluntary swallowing or peristalsis **achalasia *strokes *PD *MS *Musc Dystrophy ```
29
list the primary esophageal motility disorders
``` DIRECT ISSUE WITH ESOPH ITSELF: achalasia diffuse esophageal spasm nutcracker esophagus hypertensive LES ```
30
list the secondary esophageal motility disorders
SEQUELAE OF ANOTHER DZ: - GERD - scleroderma (collagen depositions impairs contractility) - chagas dz - post-op
31
list the mechanical dysphagia DZs
``` structural obstructions***** -Hiatal hernias -rings and webs -esoph stricture - ```
32
hiatal hernia - what is it - MC where
herniation of the viscera MC the stomach (GE junction) goes into the mediastinum -through the esophageal hiatus of the diaphragm
33
list the rings and webs
Schatzki Ring
34
Schatzki Ring - define - often assoc with? (3) - etiology
thin membranous narrowing often associated with episodic dysphagia (solids) Noncircumferential thin membrane in the UPPER/MID ESOPHAGUS--can be assoc with Zenkers *narrows the esophagus*** congenital or acqiuired Associated with: 1. episodic dysphagia to solids 2. Zenkers 3. Plummer-Vinson Syndrome: triad of dysphagia, esophageal webs and iron def anemia
35
MC type of hiatal hernia? | -explain it
sliding-- GE junction slides into the mediastinum (increases reflux)
36
esophageal stricture | -define
narrowing of the esophagus due to internal damange -often from inflammation like GERD, eosinophilic esophagitis, infection, external compression from scarring/fibrosis of mediastinum or CA
37
how long is food held in the stomach
about two hours
38
which hormone is the most effective in lowering gastric pH
pepsin
39
which hormones stimulate proton pump to secrete H+
AcH Gastrin Histamine
40
GERD can be considered a disorder of?
motility because reflux back---- causes issues with gastric emptying
41
what is GERD
*reflux of acid and pepsin from the stomach to the esophagus--**causes esophagitis** *inappropriate relaxation of LES that leads to RETROGRADE flow of stomach contents into the esophagus *abdominal pressure or delay gastric emptying can contribute to the development of reflux esophagitis *multifactorial problem *
42
GERD is often associated with?
hiatal hernias
43
Which CN brings sensory and motor innervation to pharynx and larynx?
VAGUS
44
define gastroparesis
delayed gastric emptying in the absence of mechanical gastric outlet obstruction
45
gastroparesis assciated with? (3)
DM surgical vagotomy fundoplication-- **basically anything to damage vagus nerve
46
what is the pacemaker of the stomach
Vagus nerve
47
Upper GI bleed * anatomic locations * causes
esophagus duodenum stomach Causes: * tears * ulcers * varices * severe gastritis
48
Lower GI bleed * anatomic locations * causes
Jejunum, ileum, colon, rectum
49
Melena suggests
UGIB-- the stomach digested the protein in the blood
50
Hematochezia suggsets (2)
RAPID UGIB (very very large bleeding varcies for ex) or LGIB *bright red because the protein in the blood not digested
51
Mallory-Weiss Syndrome * what is it * anatomical location * what is resp for the bleeding * assoc with? * patho behind it
longitudinal superficial mucosal lacerations/tears *at the gastroesophageal (GE) junction OR at the gastric cardia aka distal esophagus * submucosal arteries responsbile--5-10% of acute UGIB * assoc with: ETOH, overeating and over 75% have a hiatal hernia, bulemic PT, severe gastroenteritis, PATHO: 1. sudden rise in intraabdominal pressure or gastric prolpase into the esophagus (incr in pressure when you retch or vomit) 2. hiatal hernias
52
Mallory-Weiss tears are the cause of ___-___% of all acute ____ GI bleeds
5-10% | UGIB
53
DDs of Mallory-Weiss syndrome includes what other diseases?
1. Reflux esophagitis 2. Medication induced esophagitis 3. infectious esophagitis
54
``` Boerhaave's syndrome AKA? *dsecribe *MC affecting where *associated with MC? ```
Esophageal Rupture ***** * FULL THICKNESS rupture * MC affecting left posterolateral wall of the lower (distal esoph) * MC etiology=esophagus perf during endoscopy w
55
what are some things that can create an increase in intraluminal pressure to lead to Boerhaave's syndrome
``` seizure childbirth coughing straining on defication/forceful valsalva weightlifting ```
56
list the different esophagitis
- reflux esophagitis (GERD) - Infectious--causes ulcerations and lesions - Eosinophilic esophagitis--chronic - drug induced/pill induced - caustic
57
Medication/pill induced esophagitis - how does it occur - typical medications tht can cause it
Prolonged pill contact with the esophagus etiologies: * NSAIDs * bisphosphonates * iron pills * BB * CCB * vit C * some ABX....doxycycline, ampicillin
58
Infectious esophagitis * MCC? * other causes
Candida*** esp in immunocomp (HIV, transplants, CA) CMV HSV
59
Eosinophilic esophagitis define | MC in who?
allergic, inflammatory eosinophilic infiltration of the esophageal epithelium MC in kids with atopic dz (asthma, eczema)
60
caustic esophagitis | define
esophagitis caused by ingestion of corrosive substances * alkali: --draino, lye, bleach) * or acids
61
Barretts esophagus | -describe the patho
esophageal **squamous epithelium** REPLACED by precancerous **metaplastic columnar cells** from the cardia of the stomach * ****precursor to Esophageal adendocarcinoma * *compliaction of chronic GERD
62
Barretts esophagus is an example of pre-cancrous state of what kind of CA
adenocarcinoma
63
what kind of epithelium is in the upper part of esophagus
Squamous epithelium
64
what type of cells replace the normal epithelium in barretts esophagus
squamous epithelium (normal) is replaced by metaplastic columnar cells from the cardia of stomach
65
what kind of epithelium is in the cardia of stomach
columnar
66
Achalasia - define - progressin - MC in what age group
*rare form of dysphagia--*ACUIRED motor disorder of the esophageal smooth muscles * idiopathic proximal degeneration of Auerbach's plexsus (myenteric plexsus)-->leads to increased LES pressure and impaired LES relaxation * loss of peristalsis * leads to smooth muscle atrophy in the middle-lower parts of esophagus MC >50
67
Zenker's Diverticulum - define anatomic location - why does it occur - MC in?
pharyngoesophageal pouch (false diverticulum) * arises in the posterior wall of the hypopharynx--just above the cricopharyngeus muscle * only involves the mucosa and possibly submucosa OCCURS because of a natural weakness of the pharynx--Killian triangle--AND with impaired opening of the cricopharyngeus muscle MC in males
68
cricopharyngeus muscle ??
UES
69
Distal/Diffuse esophageal spasm - define - patho cause
esophageal motility disorder characterized by severe **non-peristaltic** esophageal contractions (uncoodrinated contractions) caused by impaired inhibitory innervation which leads to premature and rapidly propagated contractions
70
which is increased pressure DURING peristalsis and which is increased pressure NOT DURING peristalsis
Hypercontracticle (nutcracker) esophagus--during peristalsis Distal/diffuse esophageal spasms--NOT during peristalsis
71
Hypercontracticle (nutcracker) esophagus
esophageal motility disorder - increased pressure DURING peristalsis--normally sequential contractions in the smooth muscle of esophagus) * classically known as nutcracker esophagus
72
Plummer-Vinson Syndrome: at risk for? MC in?
triad of : 1. dysphagia 2. esophageal webs 3. iron def anemia MC in women 30-60YO high risk for esophageal CA
73
Esophageal (shatzki) ring -define MC where -assoc with?
Circumferential**** diaphragm of tissue that protrudes into the esophageal lumen * ****MC at the lower esophagus--squamocolumnar junction and accompanied with hiatal hernia - assoc with corrosive esophageal injury (ingestion of bleach, etc) and eosinophilic esophagitis
74
Esophageal CA * name the two types * which is MCC worldwide? * which is MCC in US young white males
1. Squamous cell Carcinoma * MCC worldwide 2. Adenocarcinoma * MCC in US young white males
75
Squamous cell espohageal carcinoma * location MC? * RF
-usually in the mid- upper 1/3 of esophagus RF: * smoking * ETOH * WORLWIDE RF: * HPV * Poor nutrition
76
Adenocarcinoma - location - where does it start - major RF?
MC in distal esophagus--esophagogastric junction STARTS-- in the glandular tissue--from stomach the columnar cells migrate to the esophagus--changing the normal squamous epithelium to columnar/glandular tissue=BAD RF: Barretts esophagus*** smoking and obsetiy too young white males is MC
77
esophageal varices - define - complication of? - MCC?
* dilation of the gastroesophageal collateral submucosal veins * complication of portal vein htn***** this incles HTN in left gastric vein MCC: cirrhosis (adults)
78
% of patients with cirrhosis that develop esoph varices?
90%
79
percent of patients with esoph varices that end up bleeding?
30%
80
percent of patients with an esophageal bleed that die from the FIRST bleed?
30-50%
81
percent chance of a re-bleed within the 1st year of initial bleed? *what is the percent chance of dying from second bleed
70% for re-bleed | if they rebleed: 33% die
82
why does cirrhosis cause such a high mortality rate for varices
liver produces factors for blood clotting--- with cirrhosis the liver is not funct properly and the PT does not have normal amount of clotting factors-- therefore when a varicose pops-- they bleed A LOT because the body cannot clot it
83
how can the TIPS surgery for esophageal varices cause encephalopathy
the surgery connects the hepatic vein to a branch off the portal vein---- this dumps more ammonia into the body * decrease the morbidity from bleeding varices * but doesnt improve overall mortality
84
why do we put PT on BB for prophylaxsis of esoph varices
BB will decrease CO, slow HR, and decrease splanchnic blood flow *prevents splanchnic vasodilation and decreases portal blood flow which all decrease pressure**