Quiz 3 Flashcards
Esophageal atresia:
incomplete formation of the esophagus, with abnormal connection to the stomach; N/V common; typically easy to fix surgically.
Plummer-Vinson:
difficulty swallowing and esophageal webs d/t iron deficiency anemia
tx with iron supplementation
Achalasia - features:
Increased pressure at LES
diminished peristalsis in lower 1/3 of esophagus
lack of coordinated LES relaxation w/swallowing
Achalasia - Dx:
Manometry & Barium swallow (bird-beak)
Achalasia - etiology:
lymphocytic infiltration of Auerbach’s plexus
destruction of ganglion cells
mb autoimmune, toxin, or infectious cause
Nutcracker esophagus:
dysphagia d/t over-vigorous peristaltic contraction (>180mmHg)
Mallory-Weiss syndrome - features:
bleeding tears in the stomach/esophageal jct, involving the mucosa & submucosa layers (NOT muscular layer)
typically caused by vomiting, retching, and severe coughing
mimics angina, relief with nitroglycerine (like MI), but occurs anytime (doesn’t follow worse-exertion-better-rest MI pattern)
Boerhaave’s syndrome - features:
full-thickness tear or rupture of esophageal wall
allows leak into mediastinum
caused by vomiting, lye, or rupture d/t instrumentation (scope)
Diffuse esophageal spasm (DES) - features:
corkscrew esophagus
uncoordinated contractions (several segments contract simultaneously, inability to progress bolus)
intermittent dysphagia
occasional angina
Most common cause of esophagitis:
GERD
also caused by chemical injury (acid or alkaline solution)
Candida/CMV/HSV cause in immunocompromised
GERD - cause:
change in barrier btw stomach and eso
- abnormal LES relaxation
- hiatal hernia
- increased intra-abdominal pressure (pregnancy, straining)
Two types of hiatal hernia:
Sliding
Paraesophageal
Sliding hiatal hernia is:
where GE jct & upper stomach move above the diaphragm
Paraesophageal hiatal hernia is:
upper stomach moves up and alongside distal esophagus (no mvmt of GE jct; more likely to incarcerate)
Schatzki ring:
narrowing of the lower part of the eso d/t ring of mucosal & submucosal tissue
causes intermittent dysphagia &/or obstruction
A ring: above GE jct
B ring: AT the squamocolumnar jct (SQJ)
Most common - B ring
Barrett’s esophagus - features, cause:
metaplasia of cells at the distal eso - from squamous to columnar
thought to be caused by chronic acid exposure (GERD) to better withstand erosive action
increased risk of adenocarcinoma
Barrett’s esophagus - Dx:
Biopsy and histological confirmation
The metaplastic cells of Barrett’s can be two types:
gastric - similar to stomach cells, elongated columnar/goblet cells
colonic - similar to intestinal mucin-producing cells, worse prognosis, increased malignancy
Most common cause of esophageal varies:
cirrhosis secondary to portal HTN
serious risk for hemorrhage (bleed + clotting problems)
Esophageal varices are:
dilated sub-mucosal veins in the lower 1/3 of the esophagus
How are esophageal varices treated:
banding - very effective treatment, tissue eventually necroses and sloughs off.
doesn’t affect primary cause (portal HTN) so recurrence is quite common!
Caput medusa:
distended & engorged appearance of peri-umbilical veins, not typically seen w/o portal HTN
Nearly 2/3 of benign esophageal tumors are:
leiomyomas
The gold standard for dx tissue growths:
biopsy
Granular cell tumors arise from:
Schwann cells
typically benign
can develop anywhere in the body
esophagus most common GI site
Two main forms of esophageal cancer:
Squamous cell carcinoma
Adenocarcinoma (glandular mucin-producing cells)
Esophageal cancer that arises from cells in the upper esophagus:
Squamous cell carcinoma
assoc w/alcohol & tobacco use
unexpected weight loss
low albumin
Esophageal cancer that arises at the GE jct:
Adenocarcinoma
Hx of GERD & Barrett’s
Cytological features of esophageal adenocarcinoma:
increased number of mitotic figures
variable nuclear size, staining, shape
In situ means:
basement membrane is intact
only in this site
does not have the capacity to enter circulation/lymph
Congenital diaphragmatic hernia is:
an anatomical defect of the (90% left) diaphragm allowing herniation of the bowel into the thoracic cavity.
1:2000 births
mb asx, but may cause resp distress
Pyloric stenosis is:
when is dx? Ssx:
smooth muscle hypertrophy of the pylorus, causing decreased lumen size -> inc gastric pressure, backflow into eso/mouth
often presents 2-3 wks from birth
projectile vomiting, non-bilious, failure to thrive
Cytology of congenital pyloric stenosis shows:
mucosal hyperplasia
elongated, branched, & distorted pits btw edematous, abundant lamina propria
Volvulus:
a twist causing obstruction
generally d/t ligamentous laxity
Acute gastritis:
inflammation, irritation of stomach lining
gastric mucosa infiltrated with neutrophils
often accompanied by H pylori infection
The strongest association of H. pylori is with:
duodenal peptic ulcer (>85%)
H pylori - appearance:
spirochetes (curved to spiral shaped rods)
Review - sensitivity vs. specificity:
Sensitivity - true positive rate (% sick w/true dx)
Specificity - true negative rate (% healthy who tested neg)
Benign peptic ulcers - appearance:
smooth, regular, rounded edges with a flat, smooth base and radiating mucosal folds
Malignant peptic ulcers - appearance:
irregular, heaped or overhanging margins, w/ nodular & irregular mass, mb ulcerated, protruding into the stomach lumen
Most common complication of PUD:
GI bleeding
others include:
perforation of wall (gastric, duodenal)
scarring & swelling, leading to obstruction
transformation into cancer
What is the worst prognosis area for a GI perforation?
Posterior inferior, d/t location of the pancreas, which doesn’t appreciate the stomach acid
Percent of peptic ulcers that result in perforation into peritoneal cavity:
X-ray position to assess:
10%
upright (standing)
Zollinger-Ellison syndrome triad:
hypersecretion of gastric acid (d/t excess gastrin)
severe peptic ulceration (seen in 95%)
gastrinoma (non beta cell islet tumor of pancreas)
Signature appearance of Menetrier’s dz:
markedly enlarged gastric rugae
high mucus levels
low acid levels (HCl)
low plasma protein levels (albumin loss)
Two forms of Menetrier’s dz:
childhood - noted after viral (CMV) or bacterial (H. pylori) infx
adult - over-expression of TGF-alpha (transforming growth factor)
Atrophic gastritis:
chronic inflammation of the stomach mucosa, leading to loss of glandular cells.
replaced by intestinal & fibrous tissues.
low secretion of HCl, pepsin, IF
Atrophic gastritis is usually caused by: (2)
persistent infx of H. pylori
autoimmune destruction of gastric lining
AI is more likely to develop achlorhydria & gastric carcinoma!
T/F - Pernicious anemia is due to B12 deficiency from any cause.
FALSE!
Pernicious anemia is specifically referring to B12 deficiency d/t atrophic gastritis, parietal cell loss, and lack of IF.
Inherited form of atrophic gastritis characterized by immune response to parietal cells & IF:
AMAG
autoimmune metaplastic atrophic gastritis
Characteristic AMAG findings:
serum antibodies to parietal cells & IF
Gastrin exerts a trophic effect on which cells, hypothesized to lead to carcinoid tumors found in AMAG?
ECL cells
enterochromaffin-like cells (secrete histamine)
Neoplastic glands of gastric adenocarcinoma show:
mitotic figures
greater nucleus:cytoplasm ratio
hyperchromatism
Adenocarcinoma pattern in which cells are filled with mucin vacuoles that push the nucleus to one side:
Signet ring cell pattern
Rare type of gastric CA that originates in the glandular tissue lining the stomach walls? (3 possible names)
Linitis plastica
Brinton’s dz
leather bottle stomach
poor prognosis :(
MALT stands for:
mucus-associated lymphoid tissue
e.g. gastric lymphoma
The most common intestinal atresia:
Duodenal atresia (assoc. w/Down’s syndrome)
atresia: a narrowing or absence of a portion of the intestine
Failure of neural crest cells to migrate completely during fetal development of the intestine leading to constipation and obstruction:
Hirshsprung’s disease (congenital ganglionic megacolon)
typically affects a short segment of distal colon, only 5% entire colon affected
M to F 4:1
9% have Down’s syndrome
Hirshsprung’s is suspected in a newborn when:
They haven’t passed their first meconium within 48 hrs of birth (Normal - 90% w/in 24 hrs, 99% w/in 48 hrs)
Ssx of Hirshsprung’s:
green or brown vomit
abdominal swelling
gas
bloody diarrhea
definitive dx - biopsy of narrowed segment
Complete twisting of a loop of intestine around it’s mesenteric attachment site:
Intestinal volvulus
related to malrotation, which is a common precursor in infants and children, but can occur at any age
Telescoping of a part of intestine into the lumen of an adjacent portion:
Ssx:
Intussusception
triad of -
colicky abdominal pain
bilious vomiting
red “currant jelly” stool
may lead to death if not reduced in 2-5 days
Intussusception of the large bowel is usually from an intralumenal lead point, such as:
benign: adhesions, lipomas, and adenomatous polyps
malignant: adenocarcinoma, lymphoma, and metastases
Intussusception signs
- on x-ray
- on barium swallow
x-ray: crescent sign - crescent shaped lucency in ULQ w/soft tissue mass adjacent
barium: “coiled spring”
[80% treatment rate in barium enema! 5-10% recur w/in 24 hrs]
Most frequent malformation of the GI tract:
Meckel’s diverticulum - out-pouching from the intestine located in the distal ileum (usu w/in 2 ft from IC valve)
remnant of the vitelline duct
True vs. false diverticula:
True - involve all layers including muscular propria & adventitia.
False - involve only submucosa & mucosal layers [NOT muscular & adventitia]
Most common presenting sx of Meckel’s diverticula:
painless rectal bleeding, as bright red blood or melanic black stools. Usu occurs w/o warning, stops spontaneously
Majority of people with Meckel’s - ASX
Condition of having out pocketing of the colonic mucosa & submucosa d/t weakness of the muscle layer:
Diverticulosis
Ssx of diverticulosis:
- bloating
- changes in BMs (diarrhea, constipation)
- non-specific LLQ discomfort w/episodes of sharp pain/spasm
- abdominal pain -mb post-prandial
- passage of small pellet-like stools & slime, which relieves pain
One or more inflammed diverticula:
Diverticulitis
can become infected, develop abscess, or perforate
present with classic triad - LLQ pain, fever, white cell elevation
Depending on the level affected, bowel obstruction can present as:
abd pain
abd distension
vomiting (inc fecal)
constipation
Intestinal obstruction - causes:
hernia adhesions intussusception volvulus diverticular dz infectious colitis cancer
Volvulus - definition:
complete twisting of a loop of intestine around its mesenteric attachment site.
Autoimmune dz of the small intestine caused by reaction to gliadin:
Celiac dz
Celiac dz - sx:
chronic diarrhea failure to thrive fatigue anemia 2° to malabsorption mb asx sx in another organ system
Describe celiac dz:
Exposure to gliadin causes enzyme tissue transglutaminase to modify protein, immune system cross-reacts with small-bowel tissue causing inflammatory reaction.
Celiac dz leads to villous atrophy (shortening), interfering with absorption in the small intestine. Leads to deficiency of: iron, fat-soluble vitamins A, D, K, E.
Deficiency that features a 10-fold increase in celiac risk:
IgA deficiency
found in 2.3%
also increases risk of infx & autoimmune dz!
Conditions related to celiac:
- Dermatitis herpetiformis - Itchy cutaneous condition linked to transglutaminase enzyme in the skin, identical small-bowel changes.
- Recurrent miscarriage, unexplained infertility.
- Hyposplenism
Autoimmune disorders:
- DM-type autoimmune thyroiditis
- Primary biliary cirrhosis
- Microscopic colitis
Dz w/anti-gliadin abs, but no sm bowel dz:
cerebellar ataxia
peripheral neuropathy
schizophrenia
autism
Main difference btw Crohn’s & UC:
location & nature of inflammatory changes
Crohn’s - any part of the GI (mouth to anus); MC in terminal ileum; skip lesions - transmural.
UC - colon & rectum; continuous along mucosal surface; MC begins in rectum; only mucosal layer.
Presenting sx of IBD:
abd pain vomiting diarrhea rectal bleeding severe cramps/muscle spasms wt loss
Dx by colonoscopy w/bx
The colonic mucosa of active UC shows (histo):
“crypt abscesses” - neutrophilic exudate found in glandular lumens, w/intense inflammation in submucosa; loss of goblet cells & hyper chromatic nuclei w/ inflammatory atypia.
With UC there is increased risk of:
adenocarcinoma
