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DT4- Exam 2 > Gusack- GI Path X 9-Leah, DONE :)!!! > Flashcards

Gusack- GI Path X 9-Leah, DONE :)!!! Flashcards

1
Q

Normal location of esophagus (where does it run):
vertebral level of diaphragmatic penetration?
anatomic span?

A

Cricopharyngeal muscle of pharynx –> GE junction (T11/12)

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2
Q

Location of two esophageal sphincters:

A

(essentially at the top and bottom of esophagus)

upper: at cricopharyngeus
lower: at diaphragm; just proximal to GE junction

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3
Q

What determines the tone of the LES (3)?

Is it effected by vagotomy?

A
  • Ach, gastrin, serotonin

- Not effected by vagotomy

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4
Q

Five layers of the normal esophagus:

from lumen –> outward

A

mucosal epi –> lamina propia –> muscularis mucosa –> submucosa –> muscularis propia

(same as rest of GI tract)

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5
Q

Compare the mucosal and muscular GE junctions.

  • How far apart are they?
  • Which is called the “Z line”?
A

mucosal: transition from SQUAMOUS epi of esophagus to COLUMNAR epi of the stomach; aka the “Z line”
muscular: transition from distal esophagus to proximal rugae

muscular is 2-3 cm distal to mucosal

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6
Q

When a congenital esophageal condition is detected, what other conditions should be considered?

A

Congenital heart disease, often co-exist

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7
Q

Describe atresia/ TE fistula:

A

Atresia: esophagus is a non-canalized blind pouch; two segments may be present that do not join
(proximal connects pharynx, distal connects stomach, center missing)

TE fistula: connection between the esophagus and the trachea

Two conditions often co-exist

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8
Q

How many types of TE fistula/ atresia conditions exist? Describe the most common type.

A
  • A-E (five)

- Type C most common (90%); blind upper pouch, fistula between lower segment and trachea

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9
Q

Describe the findings assc with TE fistula/ esophageal atresia (at birth and later…)

A

At birth: regurgitation, aspiration; aspiration pneumonia

Later: would lead to GERD, esophagitis

*Must correct surgically early, if compatible with life.

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10
Q

Describe the location of ectopic gastric vs pancreatic tissue in the esophagus.
Which is more common?
Which is more dangerous?

A
  • gastric: postcricoid region; red-orange well demarcated inlet patch
  • pancreatic: GEJ; has ducts and acini (like pancreas!)

Pancreatic (16% endoscopies) more common than gastric (2-4%)

Pancreatic usually benign but CAN become ductal carcinoma

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11
Q 
Esophageal web:
gross appearance
location
size 
population
3 causes
A
  • mucosal protrusion w/ fibrous core
  • UPPER esophagus
  • less than 5 mm into lumen
  • women over 40
  • idiopathic (#1), radiation, or Graft v. Host Disease
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12
Q

Schatzki ring:
location
appearance
what should you compare this to?

A
  • ring just above Z line
  • has gastric epi at undersurface

(compare to webs, which are in UPPER esophagus and have a FIBROUS core)

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13
Q 
Esophageal stenosis: 
describe the 
-submucosa 
-muscularis 
-epi 
-overall esophageal lumen:

Most general cause:

A

submucosa: thickened (“sub more submucosa”)
muscularis: atrophied
epi: ulcerated
overall: esophageal opening is narrowed

Caused by: severe injury/ inflammation/ scarring

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14
Q

What are four injuries that may induce esophageal stenosis?
What should you always screen for?
Main symptom?

A
  • radiation
  • reflux
  • scleroderma (E in CREST)
  • caustic injury (lye/ poison ingestion)
  • Screen for AI disease and suicide risk

Sx: progressive dysphagia (solids–> solids + liquids)

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15
Q

Achalasia:
What are the two functional deficits of this disease?
What is its proposed cause?

A
  • Failure of LES relaxation + esophageal peristalsis
  • No food gets into stomach!
  • T cell destruction/ absence of MYENTERIC PLEXUS
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16
Q

Population that gets achalasia?
Sx?
Tx?

A
  • young adults
  • progressive dysphagia –> regurgiation and aspiration
  • esophagomyotomy/ dilation
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17
Q

Secondary achalasia causes:

  • 1 parasitic
  • 3 neuro related
  • 3 others
A
  • Chagas (T. cruzi)
  • Polio/ neuropathy/ surgical nerve ablation
  • Tumor/ amyloidosis / sarcoidosis
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18
Q

Long term achalasia may lead to what complications?

  • 4 physical
  • 1 cancer
  • 1 infectious
A
  • mega-esophagus/ diverticula/stricture/rupture
  • ^^ SCC risk
  • Candida
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19
Q

Early vs Late (3) histo appearance of achalasia?

A

Early: EOS + T cells in myenteric plexus

Late: replacement of nerves by collagen; muscular hypertrophy; mucosa has papillomatosis + basal cell hyperplasia

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20
Q

Pseudoachalasia:

what is it and how common is it?

A
  • 2-4% patients w/ achalasia sx

- Tumor (usually adenocarcinoma) invades myenteric plexus = failure of LES to relax

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21
Q

What are the two types of hiatal hernias and which is more common? Which is more dangerous and why?

A
  • SLIDING (bell shaped) v. ROLLING (paraesophageal; fundal)
  • sliding most common

**Paraesophageal more dangerous because can result in strangulation –> necrosis

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22
Q

What causes hiatal hernias?

A

-separation of diaphragmatic crura –> widening of space between crura and esophageal wall

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23
Q

How common are hiatal hernias?
Are they usually sympomatic?
What accentuates symptoms?

A

-1-20% adults
(probably under diagnosed)

  • only 9% have GERD, rest are asx
  • symptoms accentuated by increasing pressure in abdomen (obesity/pregnancy/ leaning forward)
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24
Q 
Mallory Weiss Tears: 
location
classic cause 
treatment 
most serious sequalae?
A
  • longitudinal tear at GEJ/proximal gastric MUCOSA
  • classically in alcoholics due to retching
  • supportive tx
  • esophageal rupture (boerhaave syndrome) may be lethal outcome
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25
Q

A true esophageal diverticulum (any type) must include ____?

A

all visceral layers of the alimentary tract

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26
Q

Epiphrenic diverticulum:

  • location
  • cause
  • symptoms
A
  • above LES; due to lack of proper muscle coordination (phrenic = diaphragm, so just above LOWER sphincter)
  • get nocturnal regurgitation
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27
Q

mid-esophageal diverticulum:

current belief vs. past beliefs regarding etiology

A
  • current: motor dysfunction vs congenital

- previously thought to be caused by TB/lymphadenitis

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28
Q

Zenker’s diverticulum:
location
causes
population

A
  • False diverticulum proximal to UES, posterior wall
  • Weakness in wall at pharyngeal junction, disordered fxn of the cricopharynxgeus
  • Eldery
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29
Q

Zenker’s diverticulum:

possible complications?

A
  • Regurgitation, aspiration, halitosis, ^ risk SCCA
  • May simulate a NECK MASS*

(MISTAKEN FOR CANCER IN ELDERLY)

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30
Q

How do esophageal varices form?

Describe the blood flow pattern:

A

-portal HTN –> development of collaterals between portal/ caval systems

(blood flow: portal vein –> Lt GASTRIC VEIN–> esophageal collaterals –> IVC –> heart)

I think we need to know the portal-caval anastomosis implicated here so I added Lt gastric vein

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31
Q

Two most common causes of portal hypertension and varices?

A 
#1- alcoholism 
#2- hepatic schistosomiasis 
(s. mansoni + japonicum, vs. haematobium)
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32
Q

Describe the severity of varices?

A
  • 40% die in first episode of bleeding!!!
  • half of survivors will rebleed in first year!!

BADDDDDD– don’t have clotting factors!

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33
Q

Treatment for esophageal varices? (2)

A

sclerotherapy
balloon tamponade

(kill the extra vessels)

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34
Q

Most common cause of esophagitis?

A

1- GERD

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35
Q

GERD:
usual age
possible consequences (4)

A
  • adults over 40

- esophagitis, minor bleeds, stricture, Barretts

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36
Q

Physiologically, how does GERD injure the esophagus?

A

gastric acid/ bile acid exposure = decreased restorative capacity of the esophagus!

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37
Q

**GERD Biopsy criteria (3):

A
  1. basal cell hyperplasia
  2. heightened papillae of LP
  3. intraepi eos

**NOTE: Eos in LP are NORMAL; abnormal in epi

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38
Q

Carditis:
where is the inflammation?
what are the causes?
Significance?

A
  • just distal to Z line (proximal stomach)
  • GERD or H pylori
  • incidence of gastric cardia cancer is ^^.
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39
Q

Barret’s esophagus:
appearance (micro + gross)
#1 cause
MC populations?

A
  • intestinal metaplasia with COLUMNAR AND GOBLET CELLS!; red velvety patch grossly
  • # 1 cause is GERD
  • usually seen in older white men, also kids with CF or radiation
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40
Q

What is the management for Barrett’s?

A
  • anti-reflux agents

- Biopsies (2cm) every 1-2 years to detect any dysplasia or cancer

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41
Q

Barrett’s is a major risk factor for ____ esp in ____. Definitive diagnosis depends on the presence of _______.

A
  • adenocarcinoma; white males; goblet cells
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42
Q

Describe the progression from normal epi to Barrett’s related carcinoma

A

-squamous epi –> esophagitis –> Barrett’s –> Dysplasia –> Carcinoma

*NOTE: dysplasia is NEOPLASTIC but does NOT INVADE THE LAMINA PROPIA!
Carcinoma is INVASIVE!

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43
Q

Management of low grade vs high grade esophageal dysplasia?

A
  • low: intense antireflux + surveillance (similar to Barrett’s management)
  • high: rebiopsy/second opinion; consider esophagectomy if confirmed
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44
Q
  • Four grades for Barrett’s related dysplasia?
  • When should you be conservative about making a dx of esophageal dysplasia?
  • When is low grade dysplasia less likely to become invasive?
A
  • negative, indefinite, low grade, high grade
  • if neutros are present, consider reactive changes
  • less likely to invade if less than 2 cm or at GEJ (close to stomach)
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45
Q

Eosinophilic Esophagitis:
who gets it?
what does it resemble and how do you distinguish (2 ways)?

A
  • Young white males
  • Looks like GERD but pH is not acidic
  • Does not response to anti-relux therapy
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46
Q

Aside from dysphagia, what findings are assc with allergic/ eosinophilic esophagitis? (3)

A
  • peripheral eosinophilia
  • atopy (genetic predisposition to allergies)
  • allergen skin tests +

(draw blood if suspected!)

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47
Q

Corrosive esophagitis:
histo findings (3)
complications (3)

A
  • ingestion of chemicals i.e. lye
  • hemorrhage, necrosis, +/- bacterial infection
  • progresses to: strictures, Barrett’s, rarely SCC
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48
Q

Infectious esophagitis:

  • population infected
  • common agents (3)
  • typical signs on endoscopy/ biopsy
A

immunocompromised
candida (#1), HSV, CMV
see exudate and ulceration + neutros/necrosis

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49
Q

Candida esophagitis:
what is required for dx (on microscopy)?
what do you see on endoscopy?

A
  • fungal invasion (presence of pseudohyphae)

- see “thrush” – grey/white plaques

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50
Q

CMV esophagitis:

describe the inclusions assc with CMV ulcers; where are they found?

A
  • Intranuclear w clear halo
  • Coarse granules in cytoplasm
  • Found in endothelium + enlarged stromal cells at the base of ulcers
  • Seen in columnar NOT squamous epi
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51
Q

Esophageal ulcers:

Ddx

A

CMV vs HSV

*must rule out HSV in ulcers seen in immunocompromised because can lead to rupture or dissemination!

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52
Q

Describe viral inclusions of HSV ulcers

A
  • in multinucleated squamous epi cells
  • eosinophilic, intranuclear (Cowdry A)
  • clear halo and ground glass like CMV
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53
Q

In addition to inclusion bodies, what histo finding may suggest CMV/HSV esophagitis?

A

perivascular mac aggregates

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54
Q

3 things CMV/HSV esophagitis have in common

A
  • ulcers
  • inclusions
  • perivascular macs

(HSV more dangerous, EOSINOPHILIC inclusions are in MULTINUCLEATED cells.)

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55
Q

4 Less common causes of esophagitis

A
  • radiation/ chemo
  • pills (DOXY DID THIS TO ME!)
  • intubation
  • uremia
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56
Q

SCC of the esophagus:

  • typical presentation (late or early?)
  • 3 MC sites for mets
  • 3 areas with highest incidence?
A
  • usually late stage (invasion to muscularis, nodes mets etc)
  • mets to liver, lungs/pleura
  • iran, asia, china (bc hot tea)
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57
Q

SCC vs adenocarcinoma of the esophagus:
which is most common?
Adenocarcinoma previously confused for?

A
  • SCC but the two are now nearly equal

- AC preciously dx’ed as gastric carcinoma

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58
Q

What sex and race most commonly get esophageal SCC? What section of the esophagus is usually involved?

A
  • Black males

- mid third most common

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59
Q

Causes of/ risk factors for SCC of the esophagus

  • 3 social
  • 3 dietary
  • 1 infectious
A
  • alcohol/tobacco/urban environment
  • vitamin deficiencies, nitrosamines, betel nuts
  • fungus
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60
Q

AC of the esophagus:
sex and race usually involved?
age?
usual precursor

A

white males ~50 yoa

most arise from Barretts

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61
Q

Esophageal AC:
usual presenation? (late v early)
prognosis compared to SCC?

A
  • advanced at presentation, tends to invade lymphatics

- similar prog. to SCC

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62
Q

Esophageal AC:

histo

A
  • mucin producing intestinal mucosa (like Barretts)

- may have signets, germ cells or papillary structures; signets are BAD SIGN.

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63
Q

Five regions of the stomach

A
  1. cardia
  2. fundus
  3. body
  4. antrum
  5. pylorus
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64
Q

Two key cells found in the antrum?

Two key cells found in the fundus + body ?

A

antrum: G cells, Mucous cells

funds + body: Chief cells (pepsin), Parietal Cells (HCl)

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65
Q

Heterotopic pancreas of STOMACH:

  • tissue size
  • incidence
  • common location

In what other organ was this seen?

A
  • up to 1cm; 1-2% people
  • located in atrum or pylorus

-Also seen in the lower esophagus (GEJ junction)!

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66
Q

Heterotopic pancreas:

  • gross appearance
  • histo
  • complication?
A
  • nipple like projection; may be cystic
  • acini+ DUCTS (most obvious on images)

**can get pancreatic ca in one of these jacked up locations

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67
Q

Congenital Pyloric Stenosis:

  • male or female?
  • 4 associations
  • 2 key clinical signs
A
  • 75% males
  • ^ monozygotic twins concordinance
  • Edwards (18), Turners, Esophageal atresia
  • nonbilious PROJECTILE vomiting in neonate (**1-2 wks old!)
  • visible peristalsis
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68
Q

Acquired Pyloric Stenosis:

  • male or female
  • 2 associations
  • differential diagnosis
A
  • mostly elderly males (like congenital)
  • antral gastritis or pyloric ulcers
  • Ddx: neoplastic obstruction
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69
Q

Gross appearance of pyloric stenosis?

Treatment?

A
  • 3-5cm fusiform “olive like” mass made of pyloric muscle

- pylorotomoy (cut it open)

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70
Q

Congenital Diaphragmatic hernia:

  • cause
  • usual location (left or right?)
  • what contents protrude?
  • most dangerous complication?
A

-Defective closure of the diaphragm
(failure of pleuroperitoneal folds to form)
-MC on LEFT
-Usually stomach, can be bowel/liver
-can cause pulmonary hypoplasia –> respiratory distress –> death

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71
Q

An acquired diaphragmatic hernia would be due to?

A

-trauma (rare)

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72
Q

List 5 mucosal defenses of the stomach:

Loss of these functions contribute to?

A
  • mucus
  • bicarb
  • epi barrier
  • mucosal blood flow
  • Prostaglandins

Loss of protective mechanisms –> acute gastritis

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73
Q

How does mucus function to protect the stomach? (2)

A
  • Low diffusion coefficient for H+
    (acid stays in lumen of stomach; water has higher diffusion constant)

-“Jets” send pepsin + acid through mucus layer preventing epi contact

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74
Q

How does the epi barrier protect the stomach wall? (2)

A
  • tight junctions prevent H+ backflow

- rapid growth and restoration in the setting of damage

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75
Q

How does mucosal blood flow sustain the stomach? (2)

A
  • provides O2/nutrients (like all blood?) and bicarb

- helps remove waste (like all blood?) and acid

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76
Q

How do prostaglandins protect the stomach?

A
  • ^^ mucus and bicarb
  • lower acid secretion
  • E/I vasodilation = ^^ mucosal blood flow
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77
Q

What layer of the stomach limits injury?
How long does it take a superficial injury to heal? Deep injury?
(What defines a superficial vs deep injury?)

A
  • muscularis mucosa LIMITS INJURY
  • damage limited to the mucosa (superficial) takes only hours –> days to heal
  • damage in the submucosa can take weeks
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78
Q

Describe the difference between gastritis and gastropathy:

A
  • gastrITIS: inflammation of the gastric mucosa
  • gastropathy: mucosal damage without inflammation

(Leah: not sure I understand how you get damage without any inflammation? Maybe like mechanical injury? Regardless, this is the definition he gave.
Melissa: I don’t know either. I do not recall FA or pathoma discussing this and I think he made it up. )

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79
Q

Describe the difference between an erosion and ulcer:

A

erosion: loss of the superficial epi; does not cross muscularis mucosa
ulcer: full thickness defect; extends to muscularis mucosa

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80
Q

Acute gastritis:

3 possible complications

A
  • sloughing of the mucosa (erosion)
  • hemorrhage (cause of acute GI bleed, esp in alcoholics = hematemesis, melena)
  • death due to blood loss

*Can also be mild pain/ nausea etc

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81
Q

Causes of ACUTE gastritis:

  • drugs x3
  • social x2
  • others x 4
A
  • NSAIDs, chemo, acids/alkali
  • alcohol, smoking
  • uremia
  • infection
  • ischemia/shock/stress
  • trauma
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82
Q

Aside from loss of the 5 main protective mechanisms, how might acute gastritis occur?

A

-bile reflux

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83
Q

Contrast the appearance of mild vs severe gastritis

A

mild: edema, congestion, neutros but EPI IS INTACT
severe: MUCOSAL DAMAGE, erosion, hemorrhage, fibrinous + purulent exudate

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84
Q

Chronic gastritis may cause what complications? (2)

A
  • mucosal atrophy –> intestinal metaplasia

- dysplasia –> adenocarcinoma

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85
Q 
Causes of CHRONIC gastritis? (5) 
#1?
A

1: H. pylori

  • autoimmune (pernicious anemia, Chrons)
  • alcohol/ smoking
  • post surgical/motor/mechanical
  • radiation
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86
Q

How common is chronic gastritis?

A

-50% of US pop over age 50!!

but prevalence is decreasing due to treatment

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87
Q

Chronic gastritis:

  • most common presenation?
  • 4 possible findings?
A
  • MC: mild GI discomfort
  • HYPOchloridia (destruction of parietal cells)
  • (+/-) ^ gastrin
  • peptic ulcer
  • carcinoma/ lymphoma
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88
Q

Autoimmune gastritis is rare but most commonly involves Abs against _____.

A

components of parietal cells:

  • H/K ATPase
  • gastrin receptor
  • intrinsic factor
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89
Q

Presenation of severe autoimmune gastritis? (3)

What CANT it cause?

A
  • Hypochloridia –> ANchlorhydria
    (note: chronic gastritis may have hypochlorhydria but never ANchlorydria)
  • Hypergastrinemia
  • Small subset have pernicious anemia (B12)

**CANNOT be a cause of ULCERS!! ULCERS REQUIRE ACID.

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90
Q

Autoimmune gastritis is assc with what other 3 AI disorders?

Patients with this disease are at risk for?

A

-Hashimotos, Addisons, DM1!
(MONITOR KIDS NUTRITION IN DM1!!!!)
-Gastric carcinomas, Endocrine tumors

BUT NOT ULCERS

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91
Q

Inheritance pattern for AI gastritis?
Gastric auto-antibodies: are they always symptomatic?
What two areas of the stomach mucosa are targeted?

A
  • AD
  • Not all carrier’s of Abs are symptomatic.
  • body and fundus targeted
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92
Q

Peptic ulcers penetrate the _____, which distinguishes them from ______.
They are most common in the ___ +____.

A
  • muscularis mucosa
  • erosions
  • duodenum + stomach
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93
Q

In order from least to greatest, rank the following locations of peptic ulcers:
antrum, proximal duodenum, GE junction

A 
#1 prox. duodenum
#2 antrum
#3 GEJ
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94
Q

Multiple peptic ulcers in stomach, duodenum, and even distal small intestine (ileum, jejunum) are suggestive of?

A

Gastrin Secreting neoplasm

Zollinger Ellison Syndrome

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95
Q

Peptic Ulcer Disease (PUD):
Most common in males/ females?
Incidence increasing or decreasing?
Most common age?

A
  • males more often, esp. duodenal ulcers
  • middle age/ older adults
  • incidence duodenal decreasing, gastric unchanged
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96
Q

The most common cause of both stomach and duodenal ulcers is ______.
______ is required for ulcer formation.

What other disease process is almost always present in these patients?

A
  • H pylori #1 cause!
  • ACID presence is required (but not necessarily increased acid)
  • Most all duodenal ulcer patients and ~65% of gastric ulcer patients will have chronic gastritis.
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97
Q

How does H. pylori colonize the duodenum?

A

-H. Pylori of stomach enhances acid secretion; impairs bicarb secretion –> lower pH in duodenal lumen –> favorable conditions for gastric metaplasia = site for H pylori in duodenum

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98
Q

What makes an H. pylori strain virulent?

What percentage of duodenal ulcer patients harbor this strain?

A

Cage positive–> produce VacA toxin

*Seen in 80% patients.

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99
Q

What are the four components/ layers of an ulcer, histologically

A
  1. fibrinous exudate at surface
  2. inflammatory cells (PMNs)
  3. granulation tissue
  4. fibrotic tissue at base

(may also see re-epithelialization at margins)

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100
Q 
\_\_\_\_\_ % of patients colonized with H. pylori actually get PUD.
What are 8 risk factors? 
-2 social
-2 drugs
-3 diseases 
-2 others
A

~10-20%

  • alcoholism/cirrhosis, tobacco
  • NSAIDs, corticosteroids
  • COPD, chronic renal disease, hyperPTH
  • rapid gastric emptying, stress

(& obviously having the virulent strain)

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101
Q

How might COPD increase the risk of ulcer formation? HyperPTH?

A
  • COPD: ^^ CO2 due to poor respiration –> ^ gastrin –> PUD
  • HyperPTH: ^^Ca –> ^^ gastrin production –> ^^ acid –> PUD
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102
Q

What distinguishes an ulcer from a malignant carcinoma?

What sizes and locations are also suggestive of a benign process?

A
  • ulcers: “punched out”; sharp, clean borders; leveled edges, NO heaping edges. aka: it LOOKS benign
  • 90% of benign ulcers will be less than 4 cm and close to the pyloric ring (proximal duodenum/distal stomach) BUT this is NOT diagnostic.
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103
Q

What occurs when an ulcer penetrates beyond the submucosa, mucusoa muscularis, and eventually the entire stomach wall?

A

Adhesions or perforations…

  • Base can become adherent to other organs (i.e. pancreas, liver, omental fat)
  • OR can perforate
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104
Q

What does a healing ulcer look like, grossly?

A

-scarring causes puckering of surrounded mucosa in a “radial”/ “spokelike” fashion

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105
Q

How can peptic ulcers be distinguished from acute erosive gastritis or stress ulcers?

A
  • Look at the surrounding mucosa!
  • Most peptic ulcer patients will show CHRONIC GASTRITIS changes!
  • Stress ulcers and erosive gastritis will have normal surrounding mucosa
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106
Q

In PUD: describe what a patient would tell you about the “CARTS” of “OLD CARTS”

Where might there be referred pain in the case of a perforated ulcer?

A
  • burning pain
  • worse ~1-3 hours following a meal
  • GASTRIC = worse with food
  • DUODENAL = better with food
  • worst at night

*If perforated, pain may refer to LUQ, back, chest.

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107
Q

When diagnosing an MI/ acute coronary syndrome, what should be on your differential?

A

-PUD, esp. perforated ulcer because PAIN CAN REFER TO CHEST.

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108
Q

How long does it take a peptic ulcer to heal

  • with treatment?
  • without treatment?
A

-with treatment: few weeks
-without: avg of fifteen years
(Leah: I would love to know how they know this.)

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109
Q

What is the #1 ulcer complication/ cause of 25% PUD deaths?

What is a more rare complication but the cause of 2/3 ulcer deaths?

What ulcer complication may lead to intractable vomiting?

Is malignant transformation a risk?

A
  • # 1 complication: bleeding
  • 2/3 deaths: perforation
  • scarring–> vomiting, esp in pyloric channel ulcers

-no malignancy seen in duodenal ulcers, rarely see in gastric.

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110
Q

Hypertropic gastropathy:
-gross appearance

*Grossly, what does this condition mimic?

A

-grossly: cerebriform enlargement of rugae (inside of stomach looks like brain)

Grossly, looks the same as lymphoma/ infiltrating carcinoma!

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111
Q

Hypertrophic gastropathy:

What are the three types?

A
  • Menetrier
  • Hypertrophic/hypersecretory gastropathy
  • gastric gland hyperplasia
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112
Q

Describe the cause of the following gastropthies (gastric hypertrophies):

  • menetrier
  • hypertrophic hypersecretory gastropathy
  • gastric gland hyperplasia
A
  • menetrier: mucosal epi hypertrophy, glandular atrophy
  • hypertrophic hypersecretory: parietal and chief cell hyperplasia
  • gastric hyperplasia: gland hyperplasia in the setting of ^^ gastrin (Zollinger Ellison)
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113
Q

Gastric varices:
more or less common than esophageal?
most common location?
may be mistaken for?

A
  • less common than esophageal
  • usually at GEJ
  • may be masslike/ mistakenly biopsied= bleeding = BAD.
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114
Q

A caliber persistant artery can occur nearly anywhere, including the stomach. What is it?

A

main arterial branch extends abberantly into superficial tissues; they look like a mass and are accidentally biopsied BAD

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115
Q

Gastric Polyp:
what does the term apply to?
how are they classified?
what is NECESSARY management step in evaluation of polyps?

A
  • mass projecting above mucosa
  • may actually be lipoma/leiomyoma
  • classified as neoplastic or non-neoplastic
  • MUST BIOPSY
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116
Q

1 type non-neoplastic gastric polyp?

  • most common location
  • most common co-existing condition?
A
  • hyperplastic polyp
  • # 1 site: antrum
  • usually in chronic gastritis setting
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117
Q

Describe the three histo components of a hyper plastic gastric polyp:

A
  • hyperplastic epi
  • cystic dilation of glandular tissue
  • LP has inflammatory cells and smooth muscle strands
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118
Q

Inflammatory fibroid gastric polyp:

what are the histo components?

A
  • vascularized fibromuscular tissue

- many eos

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119
Q 
#1 stomach malignancy? (90-95%)
5 less common?
A 
#1 adenocarcinoma 
can also have: lymphomas, carcinoids, GI stromal tumors, leiomyosarcoma, schwannoma
120
Q

World-wide, how common is gastric adenocarcinoma?

How does this compare to the US incidence?

A
  • 2nd most common worldwide tumor, leading cause of worldwide cancer deaths
  • 4-6 fold less common in developed countries, including the US (only 2.5% cancer deaths here)
121
Q

Two gastric adenocarcinoma types?
Which is more common in males?
Which is more common?
More severe?

A
  • intestinal (male predominance, common)

- diffuse (equal in both sexes, severe)

122
Q

Predisposing environmental factors for INTESTINAL adenocarcinoma?(4)

A
  • nitrites
  • smoked/salted/pickled foods
  • low SES –> lack of clean fruits + veggies
  • cigarettes
123
Q

Intestinal vs. diffuse adenocarcinoma of the stomach:

which arises de novo?
which comes from dysplasia?

A
  • diffuse is de novo

- intestinal is from dysplasias

124
Q

What DISEASE states/ host factors contribute to gastric adenocarcinoma risk? (6)

A
  • chronic gastritis/ H. pylori infection
  • Blood type A (susceptible to H. pylori)
  • Partial gastrectomy (bile reflux–> gastritis)
  • Gastric adenoma
  • Barrett’s (@ area of GEJ)
  • Family Hx/HNPCC
125
Q

How does chronic gastritis put patients at risk for adenocarcinoma? (2)

A
  • hypochlorhydria (^^ H. pylori risk)

- intestinal metaplasia

126
Q

Gastric adenocarcinoma:
most common locations?
least common location?
greater or lesser curvature more likely to be malignant?

A
  • antrum/pylorus most common
  • body rarely affected
  • greater curvature masses more likely than lesser curvature to be malignant
127
Q

What three characteristics are used to classify adenocarcinomas?

A

-Depth
(above submucosa= early; below= advanced)

-Macro growth pattern
(exophytic, flat, excavated, diffuse)

-Histo types: intestinal vs diffuse

128
Q

Of the macro growth patterns (exophytic, flat, excavated, diffuse), which is the most concerning gastric adenocarcinoma?

A

-Diffuse! Metastatic, from the breast or lung can take a similar form.

129
Q

Describe the intestinal v. diffuse histo findings in adenocarcinoma

A
  • intestinal: neoplastic glands, atypical mucin vacuoles

- diffuse: no glands, individual infiltrative cells arising from middle of mucosa may have signet ring variant

130
Q

Describe the appearance of signet rings in the signet ring variant of diffuse adenocarcinoma of the stomach.

A
  • mucin formation expands the malignant cells and forces their nuclei to the periphery.
  • considered a “signet-ring carcinoma” if these cells make up 50+% of the tumor.
131
Q

Gastric adenocarcinoma mets:
where is the sentinel node?
what is a krukenberg tumor?
what is a sister mary joseph nodule?

which type of gastric adenoca. (intestinal or diffuse) can cause SMJ nodule for krukenberg tumor?

A
  • sentinel node: left supraclavicular (Virchows Node)
  • krukenberg: ovarian mets (DIFFUSE TYPE)
  • sister mary joseph: subQ met in the periumbilical region (INTESTINAL TYPE)
132
Q

In what part of the world is gastric adenocarcinoma screening done?

A

-Japan (they detect 35% of these cancers early, we detect 15%)

133
Q 
#1 site for extranodal lymphoma? 
What type of lymphomas are these most often?
A
  • # 1 site: stomach (MALT lymphoma)

- nearly always B cell lymphoma but ANY type can theoretically occur (including Hodgkins, Burkitts etc)

134
Q

How are most gastric lymphomas treated?

What does treatment failure suggest (2)?

A
  • about half can be treated with abx for pylori (#1 association)
  • failure suggests trisomy 3 or t(11,18) cells
135
Q

Gastric lymphomas:

  • what do they resemble grossly?
  • what do they look like on histo?
A
  • cerebriform appearance, like Menetrier’s disease/ gastric hypertrophies
  • monomorphic lymphocytes in and around the gastric glands
136
Q

GI stromal tumors:

  • from what cells do they originate?
  • Ab stains?
  • two histo patterns?
A
  • interstitial cells of cajal
  • c-KIT, 70% also CD34+
  • spindle vs epitheliod subtypes
137
Q

Compare the normal epi of the small and large intestine:

A

Small intestine: numerous villi –> varying height

Large intestine: no villi, deep glands –> mucosa all one level
should be able to draw a semi-straight line across it

138
Q

In general, and when applied to the small intestine, what is the difference between atresia and stenosis?

A
  • atresia is a COMPLETE occlusion

- stenosis is NARROWING

139
Q

Describe the three types of intestinal atresia, and where do they most often occur?

A

-duodenum #1, jejunum + ileum equally rare, never the colon

  1. fibrous diaphragm (obstruction in lumen)
  2. complete fibrosis (two segments connected by string)
  3. complete separation (defined in phrase)
140
Q

In addition to basic developmental failure, what two intrauterine events may lead to intestinal stenosis?

What complications may result?

A

-dvlp failure/ intussusceptions/ vascular accidents –> STENOSIS –> obstruction +/-perforation –> meconium peritonitis

141
Q
  • What is the difference between heterotopic gastric mucosa and gastric metaplasia in the intestine?
  • Which is likely congenital and which is likely caused by H pylori?
  • What might this tissue cause?
A
  • heterotopic gastric mucosa: full thickness of mucosa is gastric type (congenital)
  • gastric metaplasia: only surface epi is gastric type (H pylori, response to stress)
  • Just like gastric tissue, can ulcerate/perforate/ bleed etc
142
Q

Heterotopic pancreas of the intestine:
what does it look like?
where is it most common?

A
  • just like heterotopic pancreas in the eso/stomach….
  • yellow submucosal nodule with central dimple
  • ducts and acini, no islets

*common at ampulla of vater (which makes since, because this is where the pancreatic secretions will empty into the duodenum….)

143
Q

Most common complication of heterotopic pancreas?

A

Most common complication is BLOCK of duct at ampulla of vater –> infection/FAT necrosis

BUT NOTE: this is usually not symptomatic.

**can also have neoplasm arise here

144
Q

Hirschsprungs Disease:

  • definition
  • cause
  • possible complications (2)
A

Aganglionosis (no meissner/ auerbach) of a portion of the GI tract starting at the rectum and ascending to various degrees –> FUNCTIONAL obstruction + dilation proximal to lesion

Caused by failure of cephalad –> caudad neural crest cell migration

Can lead to dilation of proximal segment: “mega colon”

145
Q

Genetic associations of Hirschsprungs:

A

-many genes, many modes of inheritance…

but note: ^^ IN DOWNS! Always check out the tummies of these kiddos.

146
Q

Contrast short and long segment Hirschsprungs disease:
Which is more common in boys? girls?
In general, which of the two is seen more often?

A
  • short: rectum + sigmoid colon only (boys)
  • long segment: rectum –> entire colon (girls)
  • Short segment/ boy version is more common.
147
Q

Absence of mural ganglion cells in Hirschsprungs is sometimes accompanied by _____?
What is the appropriate stain for detection?

A
  • Hypertrophy of non-myelinated nerve fibers in the lamina propia!!
  • Stain for AchE
148
Q

How does Hrischsprungs usually present?

List two possible early complications.

A
  • # 1 little guys don’t pass their meconium –> obstructive constipation
  • can rupture their bowel and get peritonitis!
  • may also have fluid disturbance/ enterocolitis
149
Q

Necrotizing Enterocolitis:
What is it and what causes it?
In what population is this most common and when is it seen?
what causes it?

A
  • Poor mucus barrier –> bacteria migrate into gut wall
  • Neonates after oral feeding; esp low birth weight (1/10 LBW babies)
  • Intestinal ischemia + inflammatory mediators (PAF) are needed to mediate the disease, but true etiology= controversial
150
Q

Where does necrotizing enterocolitis most commonly occur?
What does it look like?
How does it heal?

A
  • Terminal ileum, cecum, right colon
  • Distended/friable/gangrenous segment

Heals with granulation/ fibrosis shortly following episode–> strictures and lifelong trouble

151
Q

Presentation/ complications assc with necrotizing enterocolitis?

A
  • # 1: bloody stools/ abdominal distention
  • Gas in the intestinal wall (pneumatonis intestinalisis)
  • Circulatory collapse/shock/sepsis! BAD! WATCH THE TINY BABIES!
152
Q

Water:
how many liters enter the GI tract daily?
where is it absorbed?
how much water is lost in diarrhea?

A
  • ~9L intake (including drinking, bile, saliva, etc)
  • jejunum: 3-5L
  • ileum: 2-4L
  • colon: 2L

-diarrhea: loss of more than 500 mL fluid in stool/day.

**THIS IS STUPID AND ANNOYING AND WILL NOT BE TESTED ON STEP. I HATE HIM. ONLY DIARRHEA IS IMPORTANT.

153
Q 
Secretory vs osmotic diarrhea:
which stops when you stop eating?
which is isotonic with plasma?
which is often caused by viruses?
are they watery or bloody?
A
  • OSMOTIC stops with fasting
  • SECRETORY is isotonic with plasma (problem with cells; persists w fasting)
  • virus often = secretory
  • BOTH are WATERY
154
Q

Compare the osmolality of stool fluid v plasma in osmotic diarrhea:

List four possible causes of this type of diarrhea:

A

-stool is over 50 mOsm higher than plasma

  • lactase def./lactuolose therapy
  • gut lavage
  • antacids
  • bile acid malabsorption
155
Q

Exudative disease:
what kind of diarrhea?
stops on fasting?
causes? (4 infectious, 2 others)

A

MUCOSAL DISTRUCTION:

  • bloody, pus filled stool
  • PERSIST w fasting, like secretory

Causes:

  • campy, shigella, salmonella, e.histolytica
  • IBD
  • thyplitis
156
Q

Positive fat stain in stool suggests what if:
chronic?
acute?

A
  • chronic: malabsorption

- acute: travelers diarrhea, Giardia!

157
Q

Describe the appearance of the gut mucosa in bacterial enterocolitis:

A
  • ^mitoses/ immature epi (regenerative change)
  • Hyperemia/ edema of lamina propia
  • ^^Neutros in both epi/lamina propia
158
Q

Shigella:
what part of the bowel is affected?
gross appearance?

A
  • distal colon
  • enlargment of lymphoid nodules (tiny projections)
  • purulent exudate
  • late: soft/friable/ulcerated mucosa
159
Q

Salmonella:
what part of the bowel is effected?
appearance: 1 histo, 2 gross

A
  • colon AND ileum
  • MONONUCLEAR inflammation
  • Peyers patch involvement –> swelling + congestion–> LINEAR ULCERS
160
Q

Pseudomembranous colitis:
whats the bug?
what do the lesions look like?
what is the cause?

A
  • c. diff
  • mushroom like lesion, filled with neutros/fibrin
  • any abx lead to overgrowth, classically clindamycin
161
Q

C. diff:

  • gram positive or negative?
  • shape?
  • aerobic or anaerobic?
  • toxin A function?
  • toxin B function?
A
  • gram + spore forming rod
  • obligate anaerobe

-toxin A: enterotoxin + cytotoxin
(distrupts cytoskeleton, neutrophil chemotaxis)
-toxin B: cytotoxin

162
Q

Best way to detect c. diff?

A
  • endoscopy: detects only half of cases
  • toxin in stool is specific but not sensitive

…so HARD to diagnose; Yu says you can smell it….

163
Q

Describe the stool associated with malabsorption:

A
  • bulky/excess fat/ foul/floating/ greasy

- abates on fasting

164
Q

Most reliable test for malabsorption:

A

-quantitative stool analysis over 72 hours

165
Q

Celiac Disease:

  • areas affected?
  • two findings on biopsy?
  • are these specific?
A
  • Location: duodenum» jejunum + ilium
  • ^^ inflammatory cells at epi surface
  • ^^ crypt/ villi ratio (villi destroyed; crypts elongated= mucosa height normal)

non-specific, seen in many other conditions

166
Q

Where are B12 (cobalamin) and bile salts absorbed?

A

distal ileum ONLY (no plasticity here)

167
Q

Three criteria for Dx Celiacs:

Population commonly effected?

A
  1. Pt improves when gluten not eaten
  2. mucosal lesions (villi destroyed, deep crypts)
  3. malabsorption

*usually in caucasians

168
Q

Serologic tests for Celiac?

What are they and are they specific?

A

-screen for Abs against transglutaminase and gliadin (IgA»>IgG)

-CANNOT DIAGNOSE ON THIS ALONE!
(Screening tool only)

169
Q 
Tropical sprue:
area of intestine infected?
bacteria type involved?
biopsy appearance?
malabsorption?
A
  • jejunum + ilium&raquo_space; duodenum
  • gram negative overgrowth
  • short/thick villi
  • B12, fat, protein malabsorption

**Presents like celiac but infectious etiology and mostly in jejunum and ilium

170
Q

Whipple Disease:
bacteria involved?
organ systems involved?

A
  • Tropheryma Whippelli

- any organ system, usually intestine, CNS, joints

171
Q

Key micro finding assc with Whipple Disease:

cell, appearance, stain

A

MACROPHAGES!

  • distended/foamy macs in lamina propia
  • contain rod shaped bacilli
  • PAS+ w/ diastase resistant granules

**The ^^^ MQs compress central lacteals–> MALABSORPTION

172
Q

What are two of the “more gentle colitides”?

Symptoms? Gross appearance?

A
  • collagenous colitis + lymphocytic colitis
  • 3-20 BMs/day; cramping, flatulence etc.
  • normal radiographs and mucosa grossly
173
Q

Collagenous Colitis:

  • histo appearance
  • stain?
  • population
A
  • collagen deposits just below surface epi
  • collagen seen on trichrome stain
  • middle aged women
174
Q

Lymphocytics Colitis:

  • histo appearance
  • population
  • association
A
  • intraepi lymphocytes
  • males = females
  • AI disease assc
175
Q

Mechanical compromise of vasculature often leads to what kind of infarct?
Hypoperfusion often leads to?

A
  • mechanical: transmural

- hypoperfusion: mucosal (farthest from blood supply, especially at splenic flexure bc watershed)

176
Q

Arterial thrombi most often effect what part of the intestinal vasculature?
Arterial emboli?
Risk factors/ causes?

A
  • Arterial thrombi: ORIGIN of mesenteric vessels from aorta
  • Emboli: branches of the SMA

*CAUSES: THESE ARE INTUITVE! WE KNOW ATHEROSCLEROSIS –> THROMBI

(No need to memorize his huge lists. We know these things if we use our noggins.**I LIKE YOUR STYLE)

177
Q

Venous thrombi, as opposed to arterial, are often caused by what things?
Number one assc malignancy?

A

-Hypercoagulable States
(OCPs, anti-thrombin 3 def, neoplasms, sepsis, trauma, cirrhosis)

-NOT part of typical atherosclerosis

***Hepatocellular carcinoma = important neoplastic cause of intestinal venous thrombi; note these occur in SMV and IMV

178
Q

Non-occlusive ischemia causes?

4 disease states, 1 medicine combo

A

-CHF, shock, dehydration, vasoconstriction
(loss of fluid, decreased perfusion, intuitive)

-Propanolol + digitalis= common combo, bad for vasoconstriction + intestinal ischemia!

179
Q

Two phases of intestinal ischemic injury?

What part of the intestine is at greatest risk of infarction (and hypoperfusion!)?

A

-Initial hypoxia–> Secondary reperfusion (most severe)

-splenic flexure of colon
watershed area between SMA/IMA

180
Q
  • Gross appearance of intestinal infarcts: early and late

- How are arterial v. venous infarcts different?

A
  • 1st: congestion/ ecchymotic discoloration
  • Later: edema/ hemorrhage/ sanguineous mucus (REPERFUSION INJURY!!!)
  • Arterial: sharper borders than venous infarcts!
181
Q

Chronic ischemia:

  • may clinically mimic?
  • ….but can cause?
A
  • mimics: IBD
  • can perforate –> 50-75% death rate!!
  • window between severe sx and perf is SHORT so it is often TOO LATE!
182
Q

Population to suspect chronic intestinal ischemia in?

A

older patients with cardiopulmonary diseases or pre-existing bowel conditions

183
Q

Findings assc with bowel perforation?

A
  • diminished bowel sounds
  • board-like rigidity of ab muscles
  • N/V
  • shock –> collapse

*ALWAYS AUSCULTATE THE TUMMY!!!!!!
NO BOWEL SOUNDS –> ALWAYS WORRY!!

184
Q

Three specific vascular diseases that may result in intestinal ischemia?

A
  • Aortic/ mesenteric atherosclerosis –> cholesterol emboli downstream
  • Vasculitis: (PAN, Wegner, HS)
  • Amyloidosis
185
Q

Angiodysplasia:

  • This big fat word basically means what?
  • age?
  • location?
A
  • Dilated blood vessels (submucosa or mucosa) that can cause bleeding
  • after sixth decade
  • # 1: cecum, RT colon
186
Q

What is a diverticulum?
What must a congenital diverticulum have?
Most common congenital type?

A
  • Blind pouch that communicates with gut lumen
  • Congenital diverticulum has all three GI tube layers
  • # 1 congenital: Meckel
187
Q

Meckel’s Diverticulum:
caused by persistance of what structure?
role in fetus?
normal adult function?

A
  • persistant vitelline duct
  • connected fetal intestine to yolk sac
  • normally fibroses +connects umbilicus/ bowel
188
Q

Most common location for meckel’s diverticulum? Histo type?

A
  • Antimesenteric side of bowel within 2 feet of ileocecal valve
  • Usually intestinal mucosa, can be gastric/ pancreatic
189
Q

What layers are present in ACQUIRED diverticulae?
#1 location?
age group?
geographic distribution?

A
  • lack muscularis propia/ have an attenuated layer
  • usually at LEFT side of colon (sigmoid #1)
  • seen in nearly half of 60+ patients
  • more common in industrialized countries
190
Q

Histo appearance of bowel segments affected by diverticulae?

A
  • Hypertrophy of circular layer of muscularis propia + prominent taeniae coli
191
Q

What happens when diverticulae rupture?

What can this look like?

A
  • PeridiverticulITIS, infects pericolic fat –> abscesses/sinus tracts/ peritonitis
  • may inflame + resemble cancer!
192
Q

What two factors are needed to develop diverticulae?

A

-focal WEAKNESS
(located where nerves + vasa recta penetrate inner circular muscle)

  • ^^^ intraluminal PRESSURE
    (exaggerated peristaltic contractions as seen in low fiber diets/ low bulk stool)
193
Q

Signs/Symptoms of diverticulosis? (3)

A
  • “feel like I cannot empty rectum”
  • alternating constipation + diarrhea
  • rarely, massive (^^mortality) hemorrhage
194
Q

-Name the condition:
telescoping of one segment of an intestine into a distal segment
-What causes this in kids? adults?
-Whats the big deal? (Why is it dangerous?)

A
  • intussusception (follows peristaltic mvmt)
  • kids: etiology unkown, no traction point needed, sometimes follows rotavirus or mekel’s dvtlm.
  • adults: mass/tumor provides traction
  • can trap vessels –> infarction
195
Q

-Name the condition:
twisting of a loop of bowel around its mesenteric base
-most common location?
-outcome?

A
  • volvulus
  • # 1 site: sigmoid colon
  • causes infarct
196
Q
  • Carcinoid tumors are derived from what cell type?
  • Predominant location? Less common location?
  • How common are they? what age?
A
  • mucosal neuroendocrine cells
  • usually GI (small intestine»>)
  • occasionally arise in lungs
  • less than 2% colorectal cancer, but ~1/2 small intestine malignancies! (esp in sixth decade)
197
Q

Characteristic gross appearance of carcinoids?

Which carcinoids are least likely to met?

A
  • small, solid, yellow-tan mass (+ typical NE tumor histo)
  • firm due to desmoplasia –> kinking of intestine
  • rectal/ appendiceal carcinoids rarely met, others can
198
Q

What types of clinical findings may be assc with carcinoids tumors?

A

Endocrinopathies
(can secrete gastrin, corticotropin, insulin, serotonin etc)
Zollinger ellison, cushings, hyperinsulinemia, “carcinoid syndrome” are all possible

199
Q

How common is “carcinoid syndrome”?
Classic triad?
What is the cause?
What is required to get this from GI carcinoids?
Whats the classic Rx treatment for carcinoid syndrome?
How does it present in the heart?
How common is it?

A

TRIAD: Flushing, SOB, Diarrhea

  • Due to ^^ serotonin
  • HEPATIC METS REQUIRED for GI carcinoids (BECAUSE 5HT must ESCAPE HEPATIC METABOLISM to 5-HIAA!)!!!!*****
  • Tx with octreotide

Carcinoid Heart Disease: RIGHT HEART ONLY (Lung has MAO, metabolizes 5HT before getting to Lt heart)

Only 1% of localized carcinoids, 20% with widespread mets

200
Q

Three types of B cell GI lymphomas

A
  • MALT lymphoma
  • Burkitts
  • Immunoproliferative Small Intestinal Disease (IPSID)
201
Q

MALT Lymphoma:

  • Most common location in GI tract
  • Most common geographic location
  • Translocation
  • CD markers
A
  • anywhere is possible but 55-60% focal stomach lesion
  • Adults of western hemisphere
  • t(11,18)
  • NEGATIVE for CD5,10
202
Q

Immunoproliferative Small Intestinal Disease:

  • aka?
  • seen in pt’s w/ history of?
  • etiological cause/ what precedes lymphoma?
  • age group?
A
  • Mediterranean lymphoma
  • chronic diffuse mucosal plasmacytosis
  • abnormal IgA chain –> malabsorption/ weight loss –> lymphoma
  • kids and young adults
203
Q

T cell lymphoma:

  • commonly assc with?
  • age group?
  • part of bowel effected?
  • outcome?
A
  • assc with long-term malabsorption syndromes
  • THINK CELIAC*
  • young adults and teens
  • small intestine
  • poor prognosis (11% survival)
204
Q

Five mesenchymal tumors of the GI tract?

A
  • lipomas (submucosa intestines)
  • lipomatous hypertrophy (ileocecal valve)
  • leiomyomas
  • leiomyosarcomas
  • Gastrointestinal stromal tumors (GISTs)
205
Q

Type of tumor seen in the anal canal?

Three subtypes?

A

Carcinomas

Patterns: basaloid, squamous, adenocarcinoma

206
Q

Basaloid anal carcinoma:

from what cells is it derived?

A

basal layer of stratified squamous epithelium

207
Q

Squamous cell carcinomas:

2 associations

A

HPV, Immunosupression (AIDS, transplant)

208
Q

Appendicitis:

what is the sequence of events?

A

-obstruction (by “fecalith”) –> increased intraluminal pressure –> collapse of the draining veins –> ischemia –> bacterial proliferation

Fecalith = stone of poops (according to google)!! :)

209
Q

Describe the gross and micro appearance of early acute appendicitis:

A

micro: neutrophils in all three GI layers/ perivascular neutros
grossly- dull red membrane (no longer glistening)

210
Q

Describe the gross and micro appearance of late appendicitis (acute “suppurative” appendicitis):

A
  • fibropurulent reaction over serosa

- abscess formation, ulcerations, necrosis

211
Q

What condition occurs if suppurative appendicitis is left untreated?

A

-acute gangrenous appendicitis –> rupture + peritonitis

212
Q

Only criteria for dx of appendicitis?

A

-neutros in muscularis propia

213
Q

When a “fibrotic” appendix is found, what could be the possible causes?

A

-congenital
OR
-chronic appendicitis

214
Q

Most common appendiceal tumor?

A

Carcinoid tumor in the distal tip

215
Q

What is a mucocele?
MOST COMMON cause?
Treatment?

A
  • enlarged appendix full of mucus
  • USUALLY caused by obstruction
  • self limiting (mucus glands atropy), usually asx
216
Q

Two possible tumors causing mucocele?

Which is: benign? malignant? rare?

A
  • mucinous cystadenoma (benign)

- mucinous cystadenocarcinoma (malignant, very rare)

217
Q

Untreated mucinous cystadenocarcinoma may lead to?

A

fills the abdomen with mucus =

“pseudomyxoma peritoneii”

218
Q

Mucinous neoplasm of the appendix in female should always lead you to check for….

A

similar ovarian cancer

219
Q

Term for eating ice, clay, starch, ice, hair etc. ?

Causes?

A

PICA/ Pagophagia

-can be seen in many things including anemia + pregnancy

220
Q

How does anemia effect the cardiac exam (BP, HR, Heart sounds?)

A
  • low BP
  • tachycardia
  • widespread midsystolic ejection murmur (less viscous blood)
221
Q

What happens when iron deficiency anemia is treated with iron?

A

Underlying cause (if not dietary) may be masked.

222
Q

Regarding GI ROS, what is one question to avoid asking your patients?

A

-Do you have diarrhea?
(Onset can be insidious, patients may not realize they have abnormal stools)
-Instead ask about the characteristics of the stool (frequency, consistency, color etc.)

223
Q

How might IBD symptoms appear in terms of timing in a female?

A
  • Diarrhea and bleeding may occur with timing of menses

- Could lead physician to mistake condition for endometriosis

224
Q

What are some causes of hypocalcemia? (5)

A
  • HypoPTH
  • low vitamin D
  • malabsorption
  • citrated blood transfusion
  • sepsis/ severe illness
225
Q

Electrolyte disturbances caused by severe diarrhea? (2)

A
  • hypokalemia

- metabolic acidosis

226
Q

Location of Chron’s Disease lesions vs. UC:

A
  • Chrons: skip lesions throughout intestine (primarily ileum and colon); may have STRING LIKE APPEARANCE (from fibrotic lesions, narrow lumen)
  • Ulcerative Colitis: continuous lesion in colon (ascending from rectum)
227
Q

Secondary lesions (type) assc with Chrons vs. UC

A
  • Chrons: uclerations/ FISSURES/ adhesions/ CREEPING FAT etc.
  • UC: secondary lesions rare
228
Q

What is colazal?

What are some pertinent ADRs?

A
  • Prodrug converted to mesalamine (5-ASA) in colon; anti-inlammatory; treats IBD
  • Can itself cause abdominal pain + diarrhea in small subset of patients ~5-6%
229
Q

Population that frequently suffers from IBD?

A
  • young, intelligent, caucasians in developed nations

- 5x incidence in European Jews

230
Q

List four of the most serious sequelae of IBD?

A
  • increased cancer risk
  • hemorrhage
  • perforation
  • toxic megacolon
231
Q

IBD- genetic associations?

A

-many have been made, penetrance incomplete!

232
Q

IBD- immunological cause?

A

Excess T cell activation –> ^^^ mucosal immune response + supression of immunoregulation

233
Q

How is the epithelial barrier of the gut affected in: Chrons? UC?

A
  • Chrons: loss of tight junctions, loss of trans-epi transport, abnormal paneth cells
  • UC: inhibited MMPase9 = defective mucin barrier
234
Q

Smoking: How does it alter the risk of Chrons? UC?
Appendicitis: how does it change the risk?

A

-Chrons: increased risk
-UC: smoking is protective
(true story, I have a friend with UC, and the doctor actually TOLD him he should smoke. WOW!!)

-Appendicitis: lowers UC risk

235
Q

Bowel wall in:
Chrons?
UC?

Which has transmural effect and which is above m. mucosa?

A
  • Chrons: thick (fibrosis) and rubbery (serositis)
  • UC: thin and pliable, reflective (shiny) areas, pseudopolys* and ulcers*
  • Chrons: transmural
  • UC: above m. mucosa
236
Q

Mucosal surface in:
UC?
Chrons?

A

UC: top heavy inflammation; CRYPTITIS/ crypt abscesses; paneth metaplasia

Chrons: “cobblestoning”; mixed inflammation: EOS, lymphoid hyperplasia, +/-granulomas**

237
Q

Chrons vs. UC:

  • Which has fever, more pain, and weight loss?
  • Which more often has rectal bleeding?
A
  • Chrons: more severe pain/ weight loss etc.
  • UC: more rectal bleeding

(but both can have anemia/ metabolic and volemic changes)

238
Q 
Chrons vs. UC? 
Proctitis almost always occurs in?
Pancolitis is more common in?
Torsion/instussusception/obstruction/fistulae (mechanical problems) are more common in? 
Appendicitis can occur in which?
A
  • Proctitis: UC
  • Pancolitis: UC
  • Mechnical Problems: Chrons
  • Appendicitis: Chrons
239
Q

Obstruction in a patient with UC means?

A

toxic megacolon!

240
Q

Two conditions that may mimic IBD?

A
  • malignancy

- diverticulosis

241
Q

Four types of colitis caused by known insults?

A
  • chemical colitis (resolves on w/draw)
  • radiation colitis (hx of radiation)
  • ischemic colitis (intermittent if chronic)
  • infectious colitis (self-limiting)
242
Q

How does radius of your biopsy change its volume?

A
  • small drop in radius –> large volume drop
  • because V= (4/3)(pi)(r^3)
  • small radius –> submucosal tissue usually absent

(= POOR INTERPRETATION)

243
Q

Chrons vs. UC

  • Which increases the risk of malignancy more?
  • Which causes fat and vitamin malabsorption
  • Which is essentially “cured” by surgery?
A
  • Chrons= malignancy, fat/ vitamin malabsorption AND is NOT always cured by surgery
  • In UC, colorectal removal is curative
244
Q

What conditions may occasionally be associated with both UC and Chrons?

A
  • skin disease

- arthritis/ arthrosis

245
Q

Chrons vs UC:

  • Which is often PANCA + ?
  • Which is often ASCA +?
A
  • Chrons: ASCA +

- UC: P-ANCA +

246
Q

What does the stool look like in Chrons disease?

What age group is it common in?

A
  • “pudding like”; fowl odor

- 50+ (remember, UC seen in younger humans!)

247
Q

Chrons:
location in body
assc risk?

A

-skip lesions throughout intestines (#1 ILEUM), occasionally higher (eso, stomach, mouth)

-100x greater risk of ileal adenocarcinoma
(but note: this is still a SMALL chance)

248
Q

Chrons:

what assc health conditions may be present? (5)

A
  • joint disease (always work RA up for Chrons!)
  • eye disease (episcleritis, iritis, etc)
  • skin involvement/ leg phlebitis
  • other organ systems effected (liver, pancreas, renal)
  • stomatitis/ apthous ulcers
249
Q

STRING SIGN/CREEPING FAT:

WHAT DISEASE?

A

Chrons

250
Q

Negative Fecal Occult Blood Test (FOBT) should be followed by?

A

-serial repeat FOBT

in the case that you EXPECT bleeding, of course

251
Q

On endocscopy, what makes an ulcer suspicious for malignancy?

A

-“rolled up” edges, loss of mucosal folds

252
Q

When diagnosing an adenocarcinoma through biopsy, what should you beware of?

A
  • you may get well-differentiated AND poorly differentiated pieces of tissue!
  • must look at MULTIPLE pieces/ large sections to find de-differentiation
253
Q

How does adenocarcinoma of the bowel appear on CT?

A

-irregular bowel wall thickening
(looks like grey shaddow around bowel loop)
-possible ulcer

254
Q

How might pericolic tissues be affected in adenocarcinoma of the colon?

A

-ADHESIONS!

tumor may invade/ adhese to organs/ fat/ even vessels if high grade

255
Q

What should you remember when your patient is given a TMN stage?

A
  • Morphologic features of tumor are often more important than the stage itself.
  • Tumor may be MORE or less invasive than stage suggests, so be careful about giving a prognosis
256
Q

Hamartomas and Juvenile Polyps are often assc with____?

A

Hereditary disorders;
Hamartomas assc with conditions that have EXTRAINTESTINAL features
Juvenile polyps usually = conditions limited to GI/ skin tumors

257
Q

What is a hamartoma?

A

Benign, disorganized collection of mature tissue normally found in colon (glands, fat etc)… in my mind, similar to a teratoma

258
Q

Inflammatory polpys are assc with?

Malignant?

A

Solitary Rectal Ulcer Syndrome, no malignant transformation

259
Q

Peutz- Jeghers: age group? findings?
Cowden Syndrome: age group? findings?
Both: Hereditary?

A

Both= hereditary

Peutz- Jeghers:

  • adolescents
  • hamartomas + hyper pigmentation
  • hamartomas in GI TRACT ONLY
  • ^^^ MALIGNANCY

Cowden:

  • kids/ adolescents
  • colonic AND extra-GI hamartomas
  • ^^ BENIGN + MALIGNANT TUMORS
260
Q

Chronkhite- Canada Syndrome:

  • age group? hereditary? prognosis?
  • organ systems effected?
  • 2 Key symptoms?
A
  • NON-hereditary; older population; half die
  • GI hamartomas; integumentary/ hematologic changes
  • vitiligo, nail splitting
261
Q

Tuberous Sclerosis:

  • age?
  • hereditary?
  • findings?
A
  • any age
  • autosomal dominant, chromsome 9
  • BENIGN hamartomas throughout GI + body; see mental retardation, etc.
262
Q

Juvenile Polyposis:

  • location polyps
  • presentation
  • age
  • micro appearance
  • extra findings in hereditary form?
A
  • polyps throughout GI, MC= rectum/ colon
  • rectal bleeding= SCARED PARENT! + anemia
  • kids
  • cystic (dilated glands); NO crowded pseudostratified cells; NO fibromuscular support
  • clubbing digits, AV malformations in lung if hereditary form
263
Q 
Peutz-Jeghers Polyps:
Mutation?
MC location of polyps?
Histo appearance of lesions?
Other assc Lesions?
A
  • AD: loss of tumor supression
  • MC: small intestine
  • arborizing CT, SM, Lamina Propia (hamartomas)
  • mucocutaneous blue-brown macules esp AT ORAL MUCOSA
264
Q

2 Risks assc with Peutz-Jeghers?

Most important step in management for Peutz- Jeghers Disease?

A

-Risk intussusception –> infarct + ^^ risk MANY cancers
-SURVEILLANCE!
THEY HAVE ^^ RISK SO MANY TUMORS!
CHECK FOR THEM!

265
Q 
Cowden Syndrome:
Mutation?
Location of polyps? 
Location of other masses? 
One special symptom?
A
  • AD lack of PTEN
  • Polyps (hamartomas) in intestines
  • ALSO MANY BENIGN/ MALIGNANT MASSES: tricholemmomas (hair follicles), skin papillomas, acral keratoses, breast/ thyroid cx etc.
  • may have MACROcephaly
266
Q

Pre-malignant polyps are almost always found where?

5 key risk factors for progression?

A

In the COLON!

  • increasing size, sessile shape
  • increasing villous component
  • increasing time from dx
  • high grade dysplasia
  • hx of invasive carcinoma
267
Q 
Villous components (bad) are often seen in what size polyp?
As such, whats the implication for biopsy?
A
  • polyps greater than 4.0 cm
  • always TAKE TUMORS THIS BIG FULLY OUT!
  • Don’t want to analyze only half because can miss the dysplastic section.
268
Q

How common are polyps in US 40 year olds?

US 60 year olds? What does this mean for colonoscopies?

A

-20% of 40 year olds
-HALF of 60 year olds
–> so start colonoscopy at age 50! ….
but so many are benign = ^^ false +

269
Q

What mechanical complications may be assc with polyps?

3

A

obstruction, torsion (acute abdomen), intussusception

270
Q

Hyperplastic polyps:

  • cause
  • most common location
  • gross appearance
A
  • low cell turnover
  • left colon
  • less than 0.5 cm, sessile
  • no nuclear crowding, mitoses, or pseudostratification
271
Q

Normal histo apperance of INTESTINAL hyperplastic polyps:

benign or malignant?

A
  • Tufts of columnar and goblet cells w/ uniform base
  • See stellate (star shaped) crypts
  • completely benign
272
Q

Tubular adenomas:
common age and location?
location?
benign or malignant? prognosis?

A
  • older adults in developed countries (diet?)
  • anywhere in colon
  • pre-malignant, MOST FOLLOW UP!
  • good prognosis IF YOU FOLLOW UP!
273
Q

Tubular adenomas:

  • size
  • gross appearance
  • two types
A
  • less than 0.5cm up to 10 cm
  • smooth and velvety, pulls the underlying CT up into polyp
  • sessile vs. pedunculated
274
Q

Describe the appearance of a pedunculated tubular adenoma? sessile?
Which is more common?

A
  • pedunculated: ball like mass at the end of a stalk, mobile

- sessile: low to flat, no dome, more common

275
Q

Tubular adenoma:
histo appearance?
pertinent negatives?

A
  • complex crowded glands, pseudostratified columnar epi
  • ^^ mitoses, loss of goblets
  • no desmoplasia in LP or penetration of m.mucosa (NO INVASION)
276
Q

Villious adenoma:

  • hereditary?
  • location?
  • how common?
  • key findings?
  • treatment of choice?
A
  • hereditary
  • proximal colon
  • less common than tubular adenomas, but MORE DANGEROUS
  • bowel perforation/ electrolyte imbalances
  • segmental colectomy
277
Q

Villious adenomas:
gross apperance
histo appearance

A
  • velvety, irregular mucosa, no stalk (looks like CARPET)
  • pulls CT up into polyp, like hamartoma, but not arborized
  • vertically aligned glands, elongated crypts, crowded + long villious projections (tubular adenoma + villi)
278
Q

Describe the difference between:

tubular, tubulovillious, + villious adenomas

A

tubular: less than 25% villous
villous: over 75% villious
tubulovillous: between

279
Q

Serrated adenoma:

  • how common?
  • location?
  • genetic changes?
  • benign or malignant? treatment?
A
  • 1-2% polpys
  • distal colon
  • microsattelite/ DNA methylation malfunction
  • 5% get adenocarcinoma; should remove
280
Q

Serrated adenoma vs hyperplastic polyp:

two differences in gross appearance

A
  • serrated adenoma = larger than hyperplastic

- also not at mucosal folds

281
Q

Serrated adenoma:

micro appearance? (4)

A
  • thickened base + LP w/ chronic inflammation
  • very enlongated crypts
  • star like appearance of glands
  • NO ^^ mitoses/ pseudostratification etc
282
Q

Familial Adenomatous Polyposis:

  • two possible mutation
  • location of polyps in both?
  • number of polyps needed for dx?
A
  • AD, APC mutation
  • AR, MUTYH mutation
  • polyps anywhere in colon
  • need 100 polyps but remember not all are necesarily visible!
283
Q

Hereditary Non-polyposis Colorectal Cancer:
location of polyps?
transmission pattern?

A
  • polyps in right colon

- AD MSH gene

284
Q

Sporadic Colon carcinoma:
two possible mutations?
location of polyps in each?

A
  • left colon; APC mutation

- right colon; MSH mutation

285
Q

Which three hereditary polyp syndromes present with serrated adenomas?

(assume others = tubular/ villious)

A

FAP (MUTYH gene)
HNPCC
Sporadic (MSH gene)

(So APC mutations = tubulovillous)

286
Q

FAP:

Aside from polyps of the colon, what lesions may be seen? (3)

A

-stomach, apulla of vater, retinal pigment hypertrophy.

287
Q

Gardner and Turcot syndrome are related to what condition? Where do they cause lesions?

A
  • Gardner: fibromas, osteomas of the mandible, supernumerary teeth
  • Turcot: brain tumors (medulloblastomas #1)
  • Both + FAP, presence of either = ^ risk FAP and vice versa!
288
Q

HNPCC:
aside from the colon, where else may there be tumors?
why are tumors often missed?

A
  • stomach, small bowel, hepatobiliary tract
  • female cancers (ovary, uterus, breast)
  • brain
  • skin

*tumors are flat and not always visible on endoscopy

289
Q

Major malignancy of the colon?
How does it progress?
Which stages are reversible?

A

-adenoCARCINoma
-process –> hyperplasia –> dysplasia –> cancer
OR DIRECTLY TO CANCER in hereditary syndromes.
-all but cancer= dysplasia!

290
Q

Common age for adenocarcinomas?
How common are colon cancer deaths?
Most common location?
Treatment?

A
  • 20% before age 50!!!!, (but most are older patients)
    (point: don’t rule out adenocarcinoma from your differential based on age)
  • 2nd leading cause of cancer deaths
  • In any part of colon
  • Segmental colectomy is curative
291
Q

What do well-differentiated vs poorly differentiated adenocarcinomas look like?

What do the mucinous type adenocarcinomas look like?

A
  • well-diff: INVASIVE tubulovillious adenoma
  • poorly-diff: few actual glands, variable cell types, signet ring cells may be seen
  • Mucinous type has cells floating in MUCIN POOLS. (VERY BAD PROGNOSIS!!!)
292
Q 
Where in the GI tract can large adenocarcinomas grow without causing obstructive symptoms?
What areas are prone to obstructions? 
#1 spot for obstruction?
A

-Cecum! Pouch! (unless at the actual ileocecal VALVE)
“Can’t See ‘em in the cecum!”

-Left and right flexures, sigmoid hair pin turn, and distal left colon are at high risk for obstruction (#1= most distal colon)

293
Q

Typical symptom of a tumor obstructing the distal colon?

A

-alternating diarrhea and constipation

294
Q

Where may adenocarcinomas easily invade?

A

-serosal reflection at the rectum

very thin- easier for tumors to get out

295
Q

How does TNM grading for adenocarcinomas work?

A
  • T1-4 based on depth of invasion and histo grade
  • N1-2 based on number of nodes
  • M0-1 based on presence of distant mets

DT4- Exam 2 (12 decks)

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