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Pathophysiology > GI: Esophagus > Flashcards

GI: Esophagus Flashcards

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
Q

define reflux

A

passage of gastric content into the esophagus

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26
Q

define dysphagia

A

difficulty swallowing

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27
Q

list two general causes of dysphagia

A

mechanical (structural) obstruction
OR
Functional (motility) disorders

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28
Q

functional dysphagia

causes?

A 
PROPULSION: 
caused by NEURONAL or muscular disorders 
-interfere with voluntary swallowing or peristalsis 
**achalasia 
*strokes 
*PD
*MS 
*Musc Dystrophy
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29
Q

list the primary esophageal motility disorders

A 
DIRECT ISSUE WITH ESOPH ITSELF: 
achalasia 
diffuse esophageal spasm 
nutcracker esophagus 
hypertensive LES
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30
Q

list the secondary esophageal motility disorders

A

SEQUELAE OF ANOTHER DZ:

  • GERD
  • scleroderma (collagen depositions impairs contractility)
  • chagas dz
  • post-op
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31
Q

list the mechanical dysphagia DZs

A 
structural obstructions*****
-Hiatal hernias 
-rings and webs 
-esoph stricture 
-
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32
Q

hiatal hernia

  • what is it
  • MC where
A

herniation of the viscera
MC the stomach (GE junction)
goes into the mediastinum -through the esophageal hiatus of the diaphragm

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33
Q

list the rings and webs

A

Schatzki Ring

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34
Q

Schatzki Ring

  • define
  • often assoc with? (3)
  • etiology
A

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
Q

MC type of hiatal hernia?

-explain it

A

sliding– GE junction slides into the mediastinum (increases reflux)

36
Q

esophageal stricture

-define

A

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
Q

how long is food held in the stomach

A

about two hours

38
Q

which hormone is the most effective in lowering gastric pH

A

pepsin

39
Q

which hormones stimulate proton pump to secrete H+

A

AcH
Gastrin
Histamine

40
Q

GERD can be considered a disorder of?

A

motility because reflux back—- causes issues with gastric emptying

41
Q

what is GERD

A

*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
Q

GERD is often associated with?

A

hiatal hernias

43
Q

Which CN brings sensory and motor innervation to pharynx and larynx?

A

VAGUS

44
Q

define gastroparesis

A

delayed gastric emptying in the absence of mechanical gastric outlet obstruction

45
Q

gastroparesis assciated with? (3)

A

DM
surgical vagotomy
fundoplication–
**basically anything to damage vagus nerve

46
Q

what is the pacemaker of the stomach

A

Vagus nerve

47
Q

Upper GI bleed

  • anatomic locations
  • causes
A

esophagus
duodenum
stomach

Causes:

  • tears
  • ulcers
  • varices
  • severe gastritis
48
Q

Lower GI bleed

  • anatomic locations
  • causes
A

Jejunum, ileum, colon, rectum

49
Q

Melena suggests

A

UGIB– the stomach digested the protein in the blood

50
Q

Hematochezia suggsets (2)

A

RAPID UGIB (very very large bleeding varcies for ex)
or
LGIB

*bright red because the protein in the blood not digested

51
Q

Mallory-Weiss Syndrome

  • what is it
  • anatomical location
  • what is resp for the bleeding
  • assoc with?
  • patho behind it
A

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
Q

Mallory-Weiss tears are the cause of ___-___% of all acute ____ GI bleeds

A

5-10%

UGIB

53
Q

DDs of Mallory-Weiss syndrome includes what other diseases?

A
  1. Reflux esophagitis
  2. Medication induced esophagitis
  3. infectious esophagitis
54
Q 
Boerhaave's syndrome 
AKA? 
*dsecribe 
*MC affecting where 
*associated with MC?
A

Esophageal Rupture *****

  • FULL THICKNESS rupture
  • MC affecting left posterolateral wall of the lower (distal esoph)
  • MC etiology=esophagus perf during endoscopy w
55
Q

what are some things that can create an increase in intraluminal pressure to lead to Boerhaave’s syndrome

A 
seizure 
childbirth 
coughing
straining on defication/forceful valsalva 
weightlifting
56
Q

list the different esophagitis

A
  • reflux esophagitis (GERD)
  • Infectious–causes ulcerations and lesions
  • Eosinophilic esophagitis–chronic
  • drug induced/pill induced
  • caustic
57
Q

Medication/pill induced esophagitis

  • how does it occur
  • typical medications tht can cause it
A

Prolonged pill contact with the esophagus

etiologies:
* NSAIDs
* bisphosphonates
* iron pills
* BB
* CCB
* vit C
* some ABX….doxycycline, ampicillin

58
Q

Infectious esophagitis

  • MCC?
  • other causes
A

Candida*** esp in immunocomp (HIV, transplants, CA)
CMV
HSV

59
Q

Eosinophilic esophagitis define

MC in who?

A

allergic, inflammatory eosinophilic infiltration of the esophageal epithelium

MC in kids with atopic dz (asthma, eczema)

60
Q

caustic esophagitis

define

A

esophagitis caused by ingestion of corrosive substances

  • alkali: –draino, lye, bleach)
  • or acids
61
Q

Barretts esophagus

-describe the patho

A

esophageal squamous epithelium REPLACED by precancerous metaplastic columnar cells from the cardia of the stomach

  • **precursor to Esophageal adendocarcinoma
  • *compliaction of chronic GERD
62
Q

Barretts esophagus is an example of pre-cancrous state of what kind of CA

A

adenocarcinoma

63
Q

what kind of epithelium is in the upper part of esophagus

A

Squamous epithelium

64
Q

what type of cells replace the normal epithelium in barretts esophagus

A

squamous epithelium (normal) is replaced by metaplastic columnar cells from the cardia of stomach

65
Q

what kind of epithelium is in the cardia of stomach

A

columnar

66
Q

Achalasia

  • define
  • progressin
  • MC in what age group
A

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
Q

Zenker’s Diverticulum

  • define anatomic location
  • why does it occur
  • MC in?
A

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
Q

cricopharyngeus muscle ??

A

UES

69
Q

Distal/Diffuse esophageal spasm

  • define
  • patho cause
A

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
Q

which is increased pressure DURING peristalsis and which is increased pressure NOT DURING peristalsis

A

Hypercontracticle (nutcracker) esophagus–during peristalsis

Distal/diffuse esophageal spasms–NOT during peristalsis

71
Q

Hypercontracticle (nutcracker) esophagus

A

esophageal motility disorder

  • increased pressure DURING peristalsis–normally sequential contractions in the smooth muscle of esophagus)
  • classically known as nutcracker esophagus
72
Q

Plummer-Vinson Syndrome:
at risk for?
MC in?

A

triad of :

  1. dysphagia
  2. esophageal webs
  3. iron def anemia

MC in women 30-60YO
high risk for esophageal CA

73
Q

Esophageal (shatzki) ring
-define
MC where
-assoc with?

A

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
Q

Esophageal CA

  • name the two types
  • which is MCC worldwide?
  • which is MCC in US young white males
A
  1. Squamous cell Carcinoma
    * MCC worldwide
  2. Adenocarcinoma
    * MCC in US young white males
75
Q

Squamous cell espohageal carcinoma

  • location MC?
  • RF
A

-usually in the mid- upper 1/3 of esophagus

RF:

  • smoking
  • ETOH
  • WORLWIDE RF:
  • HPV
  • Poor nutrition
76
Q

Adenocarcinoma

  • location
  • where does it start
  • major RF?
A

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
Q

esophageal varices

  • define
  • complication of?
  • MCC?
A
  • dilation of the gastroesophageal collateral submucosal veins
  • complication of portal vein htn***** this incles HTN in left gastric vein

MCC: cirrhosis (adults)

78
Q

% of patients with cirrhosis that develop esoph varices?

A

90%

79
Q

percent of patients with esoph varices that end up bleeding?

A

30%

80
Q

percent of patients with an esophageal bleed that die from the FIRST bleed?

A

30-50%

81
Q

percent chance of a re-bleed within the 1st year of initial bleed?
*what is the percent chance of dying from second bleed

A

70% for re-bleed

if they rebleed: 33% die

82
Q

why does cirrhosis cause such a high mortality rate for varices

A

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
Q

how can the TIPS surgery for esophageal varices cause encephalopathy

A

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
Q

why do we put PT on BB for prophylaxsis of esoph varices

A

BB will decrease CO, slow HR, and decrease splanchnic blood flow
*prevents splanchnic vasodilation and decreases portal blood flow which all decrease pressure**

Pathophysiology (13 decks)

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