ADVANCED PATHOLOGY NR 507- FINAL
EXAM QUESTIONS AND ANSWERS
pylorus - Answer-a muscle like structure that squeezes food down into the duodenum
can become scarred and lead to obstruction with gastric ulcers
the mucosa layer of the stomach lining - Answer-secrets mucosa rich in bicarbonate - it
protects the lining of the stomach from acid
has gastric pits that contain parietal cells, chief cells, and G-cells
parietal cells - Answer-secrete HCl (hydrochloric acid) and intrinsic factor
chief cells - Answer-secrete pepsinogen, which is converted to pepsin via the action of
hydrochloric acid
G-cells - Answer-releases gastrin
submucosa - Answer-on top of mucosa
contains connective tissue, nerves, and vessels
Muscularis Externa - Answer-on top of the submucosa
three smooth muscle layers: aid in peristalysis
serosa - Answer-on top of muscularis externa
outer layer of connective tissue that connects to organs
Good and Bad key players in peptic ulcer disease - Answer-Good: "defense system"
bicarb = coats and protects cells
prostaglandins = regulates perfusion to stomach and mucus to release bicarb, controls
acid amount secreted by parietal cells
Bad: "toxic system"
ulcer (H. Pylori, NSAIDs, etc) = acid penetrates mucosa = histamine released = parietal
cells release even more HCL acid = more stomach irritation
HCL acid via parietal cells + Pepsinogen via chief cells = pepsin
Heliobacter pylori - Answer-spiral shaped bacteria that is the cause of most gastric
ulcers
,produces urease which breaks down urea = ammonia & carbon dioxide = neutralizes
acid and breaks down mucosa
spreads through oral/oral or oral/fecal
NSAIDs effect on gastric system - Answer-decreases production of prostaglandins =
impacts the health of the stomach
Zollinger-Ellison syndrome - Answer-Gastrin-secreting tumor associated with ulcers =
increased stomach acid
signs and symptoms of peptic ulcer disease - Answer-Indigestion & epigastric pain
(burning, gnawing or dull)
Gastric = eating food makes it worse (1-2hrs after), pain = dull & aching, weightloss,
sever: vomit = coffee grounds or frank red blood
Duodenal = eating food makes it better (3-4 hours after), wake in the middle of night
with pain, gnawing pain, severe: tarry dark stool
diagnosing peptic ulcer disease - Answer-scope of the stomach
upper GI series: drink barium to coat upper GI tract
CT scan of abdomen with contrast
H. Pylori = blood test, stool test, Urea breath test
Urea breath test - Answer-Patient ingests Urea with radio labeled Carbon
Measures exhaled radio labeled Carbon
Complications of peptic ulcer disease - Answer-GI bleeding = erodes a hole in stomach
= perforation = peritonitis
bowel blockage @ pylorus from chronic ulceration
increased risk for GI cancer
treatments for peptic ulcer disease - Answer-PPIs, H2 receptor blockers, antibiotics,
antacids, bismuth subsalicylates
severe cases with complications: vagotomy, pyloroplasty, gastric resection
vagotomy - Answer-cutting of certain branches of the vagus nerve, to reduce the
amount of HCL produced by the gut
pyloroplasty - Answer-surgical repair of the pylorus
,gastric resection - Answer-partial removal and repair of the stomach
-watch for dumping syndrome = cant regulate movement of food effectively = enters too
fast into intestines = food acts hypertonically pulling water from blood (early) and (late)
rich in carbs & sugar = pancreas releases insulin = hypoglycemia
Chrones disease - Answer-A form of inflammatory bowel disease, symptoms include
Crampy abdominal (right lower quadrant area) pain Fever Fatigue Loss of appetite Pain
with passing stool (tenesmus) Persistent, watery diarrhea Unintentional weight loss -
can occur throughout the digestive system - from mouth to anus. Non-continuous
manner = skip lesion
most often found in terminal illium, colon, and other areas of small intestine
has a cobblestone appearance when visualized
transmural inflammation = goes through all three layers of intestinal wall
non-caseating granulomas = sign of chronic infection
Fistula formation occurs when worsening inflammation results in tunneling between two
structures with the lumen of one section of bowel in communication with a different
section of bowel. A fistula location can be anywhere a lesion is adjacent to an area
Obstruction, malabsorption of vitamins A, D, B12, can become cancerous
Pharmacological management may include the use of aminosalicylic acid (5-ASA),
corticosteroids, immunomodulating drugs, biologic therapies, and Janus kinase
inhibitors.
ulcerative colitis - Answer-a chronic condition of unknown cause in which repeated
episodes of inflammation in the rectum and large intestine cause ulcers and irritation
Bloody diarrhea is the hallmark sign of ulcerative colitis, -abdominal cramping,
-fecal urgency and tenesmus (a continual or recurrent inclination to evacuate the
bowels).
Extra-intestinal symptoms may also be present such as arthralgias, arthritis, iritis or
uveitis, aphthous skin lesions, or gallstones.
continuous disease - does not skip areas along the intestinal tract. begins in rectum and
travels backwards to sigmoid colon - can travel to the entire colon
Smooth walls - friable appearance - looks like it will easily bleed
, inflammation of mucosa & submucosa layers of intestines only
non-caseating granulomas = sign of chronic infection
Pseudo-polyp formation occurs with worsening inflammation causing thinning of the
mucosal and submucosal layers in an uneven pattern. Has the appearance of a polyp
protruding out of the intestinal wall, but not an actual growth
Pharmacological management may include the use of aminosalicylic acid (5-ASA),
corticosteroids, immunomodulating drugs, biologic therapies, and Janus kinase
inhibitors.
Erythema Nodosum - Answer-inflammation of subcutaneous tissues resulting in tender,
erythematous nodules; may be an abnormal immune response to a systemic disease,
an infection, or a drug
can be a symptom of ulcerative colitis and chrones disease
Extra intestinal manifestations of chrones disease and ulcerative colitis - Answer-
Erythema Nodosum, migrating joint pain, redness of the eyes, & liver disease
laboratory tests for inflammatory bowel disease - Answer-increased WBCs
increased sedimentation rate
increased c-reactive proteins
anemia (low hemoglobin count)
terminal illium involvement = unable to absorb vitamin B12 = unable to make RBCs =
anemia
malabsorption = decreased albumin levels
Radiographic studies for inflammatory bowel disease - Answer-barium enema = barium
inserted through the rectum and x-ray taken - shows areas of inflammation
Risk factors for GERD - Answer--Obesity
-Hiatal Hernia (traps gastric contents above the diaphram)
-Drugs or chemicals that relax the LES (antibiotics, Ca channel blockers, bisphosphates
-pregnancy
symptoms of GERD - Answer-burning or reflux 30-90 min after a meal
symptoms worsen in reclining position
symptoms are better in upright position
symptoms improve with an antacid
Sour taste, lump in the throat, cough, hoarseness, worsening asthma episodes,
epigastric pain and chest pain may also be reported.
EXAM QUESTIONS AND ANSWERS
pylorus - Answer-a muscle like structure that squeezes food down into the duodenum
can become scarred and lead to obstruction with gastric ulcers
the mucosa layer of the stomach lining - Answer-secrets mucosa rich in bicarbonate - it
protects the lining of the stomach from acid
has gastric pits that contain parietal cells, chief cells, and G-cells
parietal cells - Answer-secrete HCl (hydrochloric acid) and intrinsic factor
chief cells - Answer-secrete pepsinogen, which is converted to pepsin via the action of
hydrochloric acid
G-cells - Answer-releases gastrin
submucosa - Answer-on top of mucosa
contains connective tissue, nerves, and vessels
Muscularis Externa - Answer-on top of the submucosa
three smooth muscle layers: aid in peristalysis
serosa - Answer-on top of muscularis externa
outer layer of connective tissue that connects to organs
Good and Bad key players in peptic ulcer disease - Answer-Good: "defense system"
bicarb = coats and protects cells
prostaglandins = regulates perfusion to stomach and mucus to release bicarb, controls
acid amount secreted by parietal cells
Bad: "toxic system"
ulcer (H. Pylori, NSAIDs, etc) = acid penetrates mucosa = histamine released = parietal
cells release even more HCL acid = more stomach irritation
HCL acid via parietal cells + Pepsinogen via chief cells = pepsin
Heliobacter pylori - Answer-spiral shaped bacteria that is the cause of most gastric
ulcers
,produces urease which breaks down urea = ammonia & carbon dioxide = neutralizes
acid and breaks down mucosa
spreads through oral/oral or oral/fecal
NSAIDs effect on gastric system - Answer-decreases production of prostaglandins =
impacts the health of the stomach
Zollinger-Ellison syndrome - Answer-Gastrin-secreting tumor associated with ulcers =
increased stomach acid
signs and symptoms of peptic ulcer disease - Answer-Indigestion & epigastric pain
(burning, gnawing or dull)
Gastric = eating food makes it worse (1-2hrs after), pain = dull & aching, weightloss,
sever: vomit = coffee grounds or frank red blood
Duodenal = eating food makes it better (3-4 hours after), wake in the middle of night
with pain, gnawing pain, severe: tarry dark stool
diagnosing peptic ulcer disease - Answer-scope of the stomach
upper GI series: drink barium to coat upper GI tract
CT scan of abdomen with contrast
H. Pylori = blood test, stool test, Urea breath test
Urea breath test - Answer-Patient ingests Urea with radio labeled Carbon
Measures exhaled radio labeled Carbon
Complications of peptic ulcer disease - Answer-GI bleeding = erodes a hole in stomach
= perforation = peritonitis
bowel blockage @ pylorus from chronic ulceration
increased risk for GI cancer
treatments for peptic ulcer disease - Answer-PPIs, H2 receptor blockers, antibiotics,
antacids, bismuth subsalicylates
severe cases with complications: vagotomy, pyloroplasty, gastric resection
vagotomy - Answer-cutting of certain branches of the vagus nerve, to reduce the
amount of HCL produced by the gut
pyloroplasty - Answer-surgical repair of the pylorus
,gastric resection - Answer-partial removal and repair of the stomach
-watch for dumping syndrome = cant regulate movement of food effectively = enters too
fast into intestines = food acts hypertonically pulling water from blood (early) and (late)
rich in carbs & sugar = pancreas releases insulin = hypoglycemia
Chrones disease - Answer-A form of inflammatory bowel disease, symptoms include
Crampy abdominal (right lower quadrant area) pain Fever Fatigue Loss of appetite Pain
with passing stool (tenesmus) Persistent, watery diarrhea Unintentional weight loss -
can occur throughout the digestive system - from mouth to anus. Non-continuous
manner = skip lesion
most often found in terminal illium, colon, and other areas of small intestine
has a cobblestone appearance when visualized
transmural inflammation = goes through all three layers of intestinal wall
non-caseating granulomas = sign of chronic infection
Fistula formation occurs when worsening inflammation results in tunneling between two
structures with the lumen of one section of bowel in communication with a different
section of bowel. A fistula location can be anywhere a lesion is adjacent to an area
Obstruction, malabsorption of vitamins A, D, B12, can become cancerous
Pharmacological management may include the use of aminosalicylic acid (5-ASA),
corticosteroids, immunomodulating drugs, biologic therapies, and Janus kinase
inhibitors.
ulcerative colitis - Answer-a chronic condition of unknown cause in which repeated
episodes of inflammation in the rectum and large intestine cause ulcers and irritation
Bloody diarrhea is the hallmark sign of ulcerative colitis, -abdominal cramping,
-fecal urgency and tenesmus (a continual or recurrent inclination to evacuate the
bowels).
Extra-intestinal symptoms may also be present such as arthralgias, arthritis, iritis or
uveitis, aphthous skin lesions, or gallstones.
continuous disease - does not skip areas along the intestinal tract. begins in rectum and
travels backwards to sigmoid colon - can travel to the entire colon
Smooth walls - friable appearance - looks like it will easily bleed
, inflammation of mucosa & submucosa layers of intestines only
non-caseating granulomas = sign of chronic infection
Pseudo-polyp formation occurs with worsening inflammation causing thinning of the
mucosal and submucosal layers in an uneven pattern. Has the appearance of a polyp
protruding out of the intestinal wall, but not an actual growth
Pharmacological management may include the use of aminosalicylic acid (5-ASA),
corticosteroids, immunomodulating drugs, biologic therapies, and Janus kinase
inhibitors.
Erythema Nodosum - Answer-inflammation of subcutaneous tissues resulting in tender,
erythematous nodules; may be an abnormal immune response to a systemic disease,
an infection, or a drug
can be a symptom of ulcerative colitis and chrones disease
Extra intestinal manifestations of chrones disease and ulcerative colitis - Answer-
Erythema Nodosum, migrating joint pain, redness of the eyes, & liver disease
laboratory tests for inflammatory bowel disease - Answer-increased WBCs
increased sedimentation rate
increased c-reactive proteins
anemia (low hemoglobin count)
terminal illium involvement = unable to absorb vitamin B12 = unable to make RBCs =
anemia
malabsorption = decreased albumin levels
Radiographic studies for inflammatory bowel disease - Answer-barium enema = barium
inserted through the rectum and x-ray taken - shows areas of inflammation
Risk factors for GERD - Answer--Obesity
-Hiatal Hernia (traps gastric contents above the diaphram)
-Drugs or chemicals that relax the LES (antibiotics, Ca channel blockers, bisphosphates
-pregnancy
symptoms of GERD - Answer-burning or reflux 30-90 min after a meal
symptoms worsen in reclining position
symptoms are better in upright position
symptoms improve with an antacid
Sour taste, lump in the throat, cough, hoarseness, worsening asthma episodes,
epigastric pain and chest pain may also be reported.
