1What are the components of a normal GI (alimentary) system?
hollow tube
peritoneum
blood supply
lymphatic system
automatic nervous sys innervation
GI divided into upper and lower portion
2What are the layers of the GI from outer to inner?
Serosa
muscularis
submucosa
mucosa
3What replaces the serosa in the upper alimentary tracts?
adventitia
4What covers the outer surface of the stomach and intestines?
peritoneum (serosal surface)
5How does the GI get its blood supply?
mesentery arteries
portal system drains venous bld from small and large intestine
6What are the functions of the GI tract?
mastication
digestion
deglutition
digestion
salivary glands
absorption
excretion
processing
7How do salivary glands help the GI (generally)?
by digestive juices
8What is deglutition?
voluntary swallowing;
food enters esophagus
peristalsis
9What is peristalsis?
smooth muscle contraction
10Where does digestion begin?
in the mouth with saliva,
in stomach with HCl and gastric enzyme
duodenum: mixed with bile, pancreatic juice, intestine enz, lysis of proteins, CHO, lipids
11What is absorption in GI?
chemically digested food taken into cells of mucosa (mostly in small intestine)
12What is processing under control of?
processing is under control of neural and neuroendocrine reflexes and enzyme release
13What is the secretory product of salivary glands?
amylase
14What is the function of the salivary glands?
digestion of starch
15What are the secretory products of the stomach?
pepsin
HCl
gastrin
intrinsic factor
16What are the functions of the stomach
digestion of proteins
stim secretion of HCl
mediates absorption of B12
17What are the secretory products of the small intestine?
enterokinase
cholecystokinin
secretin
18What is the function of the small intestine?
activate pancreatic enz
stim gall bladder contraction and pancreatic secretion of bicarbs
stim secretion of pancreatic trypsin and chymotrypsin
19What is achalasia?
dilation above spasm in esophagus
cant swallow
20What is dysphasia?
abnormal or strained swallowing
21What are the general diseases of the GI tract?
achalasia
megacolon
dysphasia
achlorhydria
malabsorption
occult hemorrhage
hematemesis, hematochezia
22What is achlorhydria?
decreased HCl
23What are the overview of GI major diseases?
dental caries
infectious diseases
circulatory disorders
multifactorial disorders
obstructive disorders
functional disorders
neoplasms
24What are the dental caries of GI disease?
gum disease
25What are the infectious diseases of GI?
gastroenteritis
C. difficile
26What are the circulatory disorders of the GI?
hemorrhagic lesions
27What are the multifactorial disorders of the GI?
peptic ulcer
inflammatory bowel disease
28What are the functional disorders of the GI?
indigestion
malabsorption
29What kind of cancers are oral cancers (historically)?
squamous cell carcinoma (SCC)
30What are oral cancers related to?
chewing tobacco, smoking, alcoholism, HPV
31What do oral cancers involve?
lips, tongue, mouth
32How do oral cancers begin?
begins as dysplasia, becomes carcinoma in situ, then invasive carcinoma
33How do oral cancers morphologically present?
leukoplakia
erythroplakia
ulcer
crater
nodule
34What are the 3 major salivary glands?
parotid
submandibular
sublingual
35What is sialadenitis?
infectious or autoimmune (Sjögren's disease)
36How does sialadenitis present?
as swelling of glands or xerostomia, xeropthalmia
37What do neoplasms affect in salivary gland disease?
major or minor salivary glands (60% benign)
38What is the most common tumor in salivary gland disease?
pleomorphic adenoma
39What are the diseases of the esophagus?
dysphagia
esophageal pain
aspiration / regurgitation
atresia
hiatal hernia
achalasia
esophagitis
varices
carcinoma
40What is dysphasia?
difficulty swallowing
41What do esophageal pain stem from?
colic or retrosternal pain (heartburn)
odynophagia
42What is odynophagia?
pain during swallowing
43What is aspiration / regurgitation important in disease of esophagus?
food from oral cavity and lead to aspiration pneumonia
44What is atresia?
lack of lumen
with or without esophageal tracheal fistula
45What is hiatal hernia?
displacement of cardiac portion of stomach
46What leads to varices?
circulatory disturbance
47What is esophageal atresia?
developmental anomaly where the connection between esophagus and trachea is broken;
food cannot pass into stomach
48What is another name for hiatal hernia?
gastroesophageal reflux
49What does reflux esophagitis result in?
displacement of cardiac portion of stomach
50What causes LES hearth burn?
relaxation or weakening of the stomach;
acid flows back into esophagus
51What can alter the tone of LES?
smoking, caffeine, coughing
52When does the LES dilate / contract?
dilates (opens) when swallowing food and contracts when food is swallowed
53When does achalasia occur?
when unable to relax LES, leading to spasm of LES (dilation of esophagus prox to site of spasm)
54What does achalasia result in?
dysphagia (inability to swallow)
55What is achalasia an antithesis (opposite?) of?
LES insufficiency
56What are the most important circulatory disturbance of the LES?
esophageal varices (dilated veins)
57What is most common in portal HTN?
esophageal varices
58What can esophageal varices lead to?
hematemesis (bleeding)
59What causes esophagitis (peptic esophagitis)?
reflux of gastric juice
60What infections lead to esophagitis?
virus
fungi
bacteria superinfection
61What noninfectious can lead to esophagitis?
chemical irritants (exogenous chemicals or drugs)
62What happens when the LES becomes compromised?
reflux of ulcerations can occur
63What mediates the LES for preventing reflux of gastric juices?
pepsin and HCl
64What does esophagitis lead to?
GERD
65What causes GERD?
peptic esophagitis, inflammation, and ulceration by squamous epithelia
66What repairs GERD?
metaplastic columnar epithelia
if not repaired, can give rise to peptic ulcers
67Where are there higher incidences of carcinoma of the esophagus?
Asia, China, Africa
men > women
68What does carcinoma of the esophagus correlate with?
alcohol, tobacco abuse
69Where do carcinoma of esophagus begin?
begins in lower esophagus
70What is the prognosis for esophageal carcinomas?
2 years
71What happens when adenocarcinoma in LES develops to Barrett's esophagus?
pain in swallowing
bleeding
invasive spread to lymph nodes
poor prognosis
72What are the most important disease of the stomach?
gastritis, peptic ulcers, and carcinomas
73What is hypertrophic pyloric stenosis?
developmental , projectile vomiting due to hypertrophy in smooth muscle of pylorus
74What happens to the stomach in hypertrophic pyloric stenosis?
unable to empty stomach leading to projectile vomiting needing surgical intervention
75What s a complication of vomiting?
obstruction of the exit portion of the stomach or irritation and disturbed motor fxn of the gastric musculature → vomiting
76What does pain in hypertrophic pyloric stenosis related to?
related to ulceration of mucosa,
caustic action of HCl,
enzymatic action of pepsin in gastric juice
77What causes bleeding in diseases of stomach?
gastric ulceration leads to hematemesis or melena
78What is dyspepsia associated with?
nausea, loss of appetite, aversion of food
79What are the systemic consequences of diseases of stomach and duodenum?
chronic bleeding ulcers may cause iron deficiency anemia
80How can diseases of stomach and duodenum lead to anemia?
lack of intrinsic factor
missing gastric protein that absorbs B12
results in pernicious anemia
81What is the duration of gastritis?
short
82What are erosions in gastritis?
shallow mucosal defects
83What are ulcerations in gastritis?
deeper, superficial bleeding
84What are curling ulcers in gastritis?
profound bleeding related to severe burns of external body
ulcers can heal if circ disturbances are removed or corrected
85What are the exogenous irritants in gastritis?
chemicals, drugs, alcohol, NSAIDs, aspirin
86What are the possible causes of chronic atrophic gastritis?
elderly, h. pylori, autoimmune
87What are the immune mediated factors that can lead to chronic atrophic gastritis?
b12, pernicious anemia, intrinsic factor
88What are the general symptoms of chronic atrophic gastritis?
labels as dyspepsia (nonspecific)
89What are the symptoms of chronic atrophic gastritis?
pain (hcl pepsin)
vomiting (obstruction)
bleeding (ulceration)
dyspepsia (anormal stomach fxn)
90What are the systemic consequences of chronic atrophic gastritis?
bleeding (microcytic anemia (IDA))
pernicious anemia (lack of intrinsic factor)
91What are the characteristics of acute gastritis?
erosive and hemorrhagic
neutrophils = predom inflammatory cell in superficial epith
92What are the symptoms of acute gastritis?
no symptoms but may cause dyspepsia, anorexia, nausea and vomiting, hematemesis, melena
93What are the symptomatic therapy of acute gastritis?
acid suppression (H2 receptor antagonist)
antiemetics (metoclopramide)
94What are the shallow mucosal defects of acute gastritis?
erosions, ulcers
95How is acute gastritis defined?
sudden inflammation or swelling in the lining of the stomach
96What is the gross anatomy of acute gastritis?
diffusely hyperemic gastric mucosa
97What is seen microscopically of acute gastritis?
surface of epith / glands intact with scattered neutrophils among epith cells or within mucosal glands
lamina propria
98What is lamina propria?
moderate edema and vascular congestion
99Who does chronic gastritis affect?
older age
100Where is chronic gastritis more common?
Far east, Eastern Europe
101What is seen in chronic gastritis?
decreased secretion of pepsin,
dyspepsia
102What are the etiology and pathogenesis of peptic ulcers?
multifactorial but can be due to:
gastric juice
mucosal barrier defects
H. pylori
genetics
exposure to pepsin and HCl
103What is present in gastric juice of peptic ulcers?
HCl, pepsin
needed for ulcer development
104how would you treat gastric juice?
H2 antagonist (cimetidine)
105What are the mucosa barrier defects that lead to peptic ulcer?
stress, shock, NSAIDs, smoking
reduces mucosa resistance
106What stimulates secretion of HCl?
gastrin
107Where are the most common ulcers?
stomach of older pts and proximal duodenum
108What are the macroscopic features of peptic ulcer?
punched out lesion into deep layer
HCl keeps bottom clean of necrotic tissue
109What are the microscopic features of the peptic ulcer?
bottom of ulcer replacing the mucosa consists mostly of granulation tissue and cell debris / inflam cells
110How do peptic ulcers bleed?
from eroded mucosal bld vessels
111What is seen in the underlying tissues of peptic ulcers?
fibrosis and scarring
112What are the complications of peptic ulcer disease?
hemorrhage
pancreas penetration
perforation
Cicatrization
113What happens if peptic ulcer invades pancreas?
acute pancreatitis
114What do duodenal ulcers eventually lead to?
peritonitis due to extending
115What is Cicatrization?
excessive fibrosis, scarring can lead to stenosis
116Where are most ulcers located?
in the distal portion of the stomach and prox to duodenum
117What age do gastric ulcers affect the most?
>50 yo
118When do ulcers cause pain?
1-3 hrs after a meal or at night;
pt is able to point to pain
119What is the treatment for ulcers today?
eradication of H. pylori infection
120What are benign epith gastric tumors?
polyps, leiomyoma
121What are the 3 diff kinds of polyps?
hyperplastic, tubular, villous
122Who is at risk of gastric tumors 10X more than others?
pts with pernicious anemia
123What are the malignant gastric tumors?
adenocarcinoma (common)
lymphoma
124What country is carcinoma of the stomach most common in?
Japan (poss. nitrosamines in food or h. pylori)
125What leads to increased nitrosamines?
decreased refrigeration; bacteria converts nitrates to nitrites
126What are the forms of gastric carcinoma?
superficial
polypod-protrude in the stomach
ulcerated
diffusely infiltration (linitis plastica)
127What is the histology of gastric carcinoma?
adenocarcinoma
128Where are gastric carcinomas commonly located?
in distal part of stomach
pylori and atrium
129What are the nonspecific symptoms of gastric carcinoma?
weight loss, anemia, vomit, bleeding, weakness, irritation
130Where do you see signet ring cells?
gastric carcinoma
131What are signet ring cells?
mucin filling cytoplasm displaces the nucleus to the periphery and gives the cell the appearance of a signet ring
132Where can gastric carcinoma metastasize to?
bilaterally to ovaries
Kuechenberg's tumor
133Where does GI lymphoma original?
MALT, Peyer's patches
134What is the most common site for GI lymphomas?
stomach of older pts and proximal duodenum
135What are the diseases of the intestines?
developmental abnormalities
diverticulosis, obstructions, hernias
vascular disorders
IBS
infections
malabsorption
neoplasms
136What are the developmental abnormalities that leads to diseases of the intestines?
Hirschsprung's disease
congenital diverticular
Meckel's
137What is a sign of Hirschsprung's Disease?
marked dilation of large intestine (megacolon) notable prox to narrowing of rectum of sigmoid colon
138What leads to megacolon in Hirschsprung's disease?
abnormal innervation of rectum and sigmoid colon
139What happens in Hirschsprung's disease?
permanent spasm
no passage of feces
intramural ganglion cells do not develop
140What happens in diverticulosis of the colon?
formation of diverticular
outpouchings intestinal wall
sigmoid colon*
protrusion through muscle wall
abscess, fistula
141What are the symptoms of diverticulosis of the colon?
chronic constipation
obstructed with fecal matter
infected, bleeding
142What are risk factors for diverticulosis?
low fiber diet
straining during bowel movement
143What does perforation of diverticular lead to?
formation of pericolonic abscesses, fistulas, or pericolonic fibrosis
144What are the intestinal vascular diseases?
hemorrhoids
angiodysplasia
ischemia bowel disease
chronic ischemia
acute thrombosis of mesenteric
nonocclusive intestinal infarcts
145What are hemorrhoids and its risk factors?
hemorrhoids=dilated veins;
risk factor: pregnancy, genetics
146What are angiodysplasia?
vascular lesion of colon;
dilated thin walled vessels
serves as anastomosis between arterial and venous circ in the mucosa and submucosa of the colon
147Who is at risk for angiodysplasia?
elderly
148What happens in ischemic bowel disease?
blood flows through segments of intestine
149What causes occlusive ischemic bowel disease?
thrombi or emboli
150What causes nonocclusive ischemic bowel disease?
atherosclerosis, narrowing
151What happens when there is too much atherosclerosis in other surrounding areas?
transmural infarction of small intestine
152What is Crohn's Disease?
thickened intestinal wall,
narrow lumen
153Where is limited regional disease seen?
colon and terminal ileum; can present as acute appendicitis; numerous skip lesions
154What are the symptoms of Crohn's disease?
granuloma, fibrosis, diarrhea, weight loss, abdominal pain, bleeding
155What is the appearance of Crohn's disease?
cobblestone appearance
156What is involved in ulcerative colitis?
diffuse, entire colon
157What happens to the mucosa in ulcerative colitis?
becomes like sandpaper, bleeding, pain;
lesions increase becoming flat and pitted (football or pig skin) ;
limited to mucosa!
158What are the symptoms of ulcerative colitis?
intestinal dilation and megacolon (toxic),
left side affection
ulcerations
pseudopolyps
distortion of crypts, aggregates of leukocytes
recurrent inflammation
dysreg immune response to microbiota
159What is the most significant complications of ulcerative colitis?
regenerating foci of epith may undergo malignant transformation
160What are the enviro factors that lead to ulcerative colitis?
antibiotic use
microbial exposure early and late in life
possibly due to diet
161When is the peak incidence for ulcerative colitis?
20s and 30s, begins in late teens;
familial predisposition, extraintestinal complications
162What is the difference between Crohn's and Ulcerative colitis?
Crohn's distribution = segmental, includes ileum whereas ulcerative colitis is diffuse colon only;
no transmural, granuloma, or fistula in UC;
no megacolon in Crohn's
163What are the immunosuppressants?
azathioprine
Azasan, Imuran
mercaptopurine
Purinethol, purixan
164What are the biological response modifiers
vedolizumab, Entyvio
ustekinumab, Stelara
infliximab, Remicade
adalimumab, Humira
golimumab, Simponi
165What are the biologic response modifiers?
TNF inhibitors; work by neutralizing protein produced by immune system
166What proteins contribute to inflammation?
IL-12, IL-23
167What causes GI infections?
food poisoning
viral infections
infectious diarrhea
small-intestine infection
large intestine infection
c. difficile
168What causes small intestine infections?
e coli, v cholera, g lamblia, rotavirus
169What causes large intestine infections?
e coli, shigella, Norwalk virus, entamoeba
170What are the causes of diarrhea?
pseudomembranous colitis (overgrowth of c difficile)
exotoxin in surface of mucosa
bact toxins ingested from preformed food
lytic action of bacteria and colonization
enterotoxigenic bacteria
typhoid fever
171What is Montezuma's revenge?
enterotoxigenic bacteria
172What causes acute appendicitis?
enterotoxigenic bacteria
173What happens in acute appendicitis?
obstruction of lumen of appendix; hardened piece of feces
174What is acute infectious peritonitis?
inflam of peritoneal lining of abd cavity;
can be secondary to rupture of stomach and appendicitis
175What causes acute infectious peritonitis?
spreads infection from fallopian tubes (neiss.)
rupture of abscess
infection of pre-existing ascites
176What is acute sterile (noninfectious) peritonitis?
acute pancreatitis
due to rupture of gallbladder
edematous
exudate of fluid into abdomen
177What is the most common cause of acute sterile peritonitis?
gall stones
178How is acute sterile noninfectious peritonitis repaired?
surgically, repairing rupture
179What causes paralytic ileus?
acute peritonitis, spinal cord injury
180What is mechanical (obstructive) ileus?
atresia / stenosis
structures
intussusception
181What is intussusception?
invagination of segment into another caused by tumor
182What leads to intestinal obstruction (ileus)?
impacted feces, foreign bodies, gallstones
malignant / inflam structures
adhesions, hernias, volvulus
183What are adhesions?
scar tissue
184How do tumors and adhesions (scar tissue) lead to mechanical obstruction?
twisting or narrowing of intestines causing bowel instruction
185What is volvulus?
rotation and twisting of intestine around mesenteric attachment site
186What is an intestinal obstruction: hernia?
protrusion of abd contents through abd wall;
weakness or defect in wall
187What is the pathogenesis of malabsorption?
inability of intestines to absorb nutrients from food;
cant properly process nutrients or transport nutrients from intestine to liver;
impaired because of gastric biliary or pancreatic insuff or bact overgrowth and parasites
188How do abnormalities lead to malabsorption?
intraluminal digestion of food depends on proper secretion of digestive juices
189What are the symptoms of malabsorption?
decreased digestive juices
digestion impaired
decreased absorption of nutrients
190What diseases affect the uptake of nutrients in intestine?
intestinal disease, like Celiac Sprue or Whipple's;
systemic diseases like scleroderma and amyloidosis
191How does gastrointestinal lymphoma lead to malabsorption
problem in transport of nutrients from intestine
192What can partial resection of intestine cause?
malabsorption
193What are the causes of malabsorption syndromes?
inadequate intraluminal digestion
reduced intestinal bile salt concentration
primary mucosal absorptive defects
impeded transport of nutrients
194What diseases lead to inadequate intraluminal digestion?
exocrine pancreatic insuff
chronic pancreatitis
cystic fibrosis
195What diseases lead to reduced intestinal bile salt concentration?
impaired micelle formation
liver disease
cholestasis
abnormal bact proliferate in small bowel
post gastrectomy states
196What disease lead to primary mucosal defects?
celiac sprue
enteritis
abetalipoproteinemia
intestinal resection
endocrine and metabolic disorders
197What diseases impede the transport of nutrients?
lymphatic obstruction (lymphoma)
congestive heart disease
intestinal ischemia
198What happens in defective intraluminal digestion?
deficiency of gastric juices: post gastrectomy conditions, atrophic gastritis (stomach resection)
deficiency of bile: biliary obstruction, liver disease, Crohn's
deficiency of pancreatic juices: chronic pancreatitis
bacterial overgrowth: Giardia Lamblia
199What is celiac sprue?
hypersensitivity to gluten (gliadin): early child; lab tests for ab to tissue transglutaminase
200What are tropical sprue?
bacteria that affects visitors to tropics
201What is Whipple's disease?
bacteria infection that leads to malabsorption
202What is congenital abetalipoproteinemia?
passage of lipids into circulation
203What does short bowel syndrome do?
prevents bowel from absorbing important nutrients, fluids, including proteins, fats and vits
204What are the features of malabsorption?
anemia, bleeding;
osteopenia: calciol and VD deficiency;
amenorrhea, impotence, infertility;
purpura, dermatitis;
peripheral neuropathy
205What leads to anemia in malabsorption syndromes?
iron, folate, and B12 deficiency
206What leads to bleeding in malabsorption?
vit K deficiency
207What leads to osteopenia in malabs syndromes?
calcium and VD deficiency
208What leads to purpura and dermatitis in malabs?
VK deficiency and VA deficiency
209What leads to peripheral neuropathy in malabs?
folate and B12 deficiency
210What does malabs from defective transport lead to?
GI lymphoma
congestive heart failure with intestinal ischemia
scleroderma
amyloidosis
dec nutrients absorbed
steatorrhea
211What is steatorrhea?
malabs of fats leading to deficiency of fat soluble vitamins
212what are the classifications of intestinal tumors?
non-neoplastic polyps
neoplastic benign polyp
malignant neoplasms
213What are the kinds of non-neoplastic polyps?
hyperplastic polyp
inflammatory
juvenile
peutz-jeghers
lymphoid
214What are the neoplastic benign polyps?
tubular adenoma
villous
tubulovillous
215What are the malignant neoplasms?
adenocarcinoma
carcinoid
216What are the genetic factors in colon cancer?
familial polyposis coli
Gardner's Syndrome
HNPCC
dietary factors
interaction of carcinogens
DNA not repaired right
Red meats / fried fat
APC gene ability as tumor suppressor
217What is the pathogenesis of FAP?
adenomatous polyposis develops in older or adolescent;
multiple polyps prob evolve to adenocarcinoma
APC gene: germ line mutation
218What are HNPCC?
develop form normal mucosal
DNA repair enzyme def
allows certain mutations to persist with no repair of damaged DNA
219What happens when oncogenes (TS genes) aren't worked?
tumors develop form epith cells lining crypts and villi,
no apoptosis
undergo malig transform bc of oncogenes
polyps protrude into the lumen
220Benign intestinal masses outnumber malignant tumor ____
2fold to 3fold
221Where do most benign and malignant tumors protrude into?
lumen of intestine (because most have epithelial origin)
222Where are most malignant tumors located?
large intestine (colorectal cancer)
223What happens in pts with HNPCC?
colonic cancers do not evolve form polyps but from normal mucosa
224What is neoplastic polyps?
intestinal
tubular adenoma is pedunculated and has stalk;
sessile and has fingerlike villi projecting from base toward lumen of intestine;
increases with age
225What does right sided adenocarcinoma of the colon look like?
ulcerated;
forms intraluminal fungating of ulcerating masses
226What does the left side adenoma carcinoma look like?
narrow lumen, obstruction for passage of feces, constipation, pencil like stools, blood in feces;
produces 'napkin ring' stenotic lesions
227What is CEA?
carcinoembryonic ag
228What composes gastrointestinal carcinoids?
neuroendocrine cells that contain granules, polypeptide hormones
229What do GI carcinoids secrete?
serotonin, polypeptide hormones (causing diarrhea, hypermotility)
230What tumors metastasizing to liver causing carcinoid syndrome affect?
right side heart valves