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PHAR123 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

True or false: the pharynx is part of the lower respiratory tract

A

false
upper respiratory tract

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2
Q

Which structure closes off the trachea when we eat to prevent food from entering the lungs?

A

epiglottis

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3
Q

What is esophagitis?

A

inflammation or infection in the esophagus

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4
Q

Which individuals are more likely to experience esophagitis?

A

immunocompromised
-patients with HIV/AIDS
-immunosuppressed due to cancer therapeutics
-immunodeficiency disorders

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5
Q

Which organism is likely to cause esophagitis in immunocompromised individuals?

A

candida

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6
Q

What is the most common cause of esophageal irritation and inflammation?

A

gastro esophageal reflux disease (GERD)
-GERD may cause acid to irritate the throat, particularly at
night after laying down, and may cause coughing

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7
Q

What is a medication that can irritate the esophagus if the patient does not remain upright after administration?

A

bisphosphonates

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8
Q

True or false: swallowing disorders are esophagitis

A

false
they represent a lack of neuromuscular coordination of the voluntary or involuntary muscles associated with swallowing

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9
Q

What is a globus?

A

feeling of something stuck in the throat, often related to anxiety

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10
Q

Where does the esophagus meet the stomach?

A

lower esophageal sphincter

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11
Q

Why is the esophagus vulnerable to acid irritation?

A

the esophageal surface is not protected by thick mucous, unlike the stomach
irritation of the esophagus causes pain and erosion
eventually inflammatory changes can occur (metaplasia)

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12
Q

What is GERD caused by?

A

lax cardiac sphincter at the gastroesophageal juncture such that acid irritates the esophageal sphincter which does not have protective mucous

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13
Q

True or false: GERD is uncomfortable, affects quality of life and sleep, and it may also mimic heart attack with intense chest pain

A

true

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14
Q

What does GERD put someone at risk for?

A

Barrett’s esophagus
-metaplasia
-pre cancerous
MUST MONITOR BECAUSE BARRETT’S=RISK FOR ESOPHAGEAL CANCER

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15
Q

What are the non-pharmacological treatments for GERD?

A

weight loss
extra pillow for sleep
earlier supper
avoiding trigger foods

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16
Q

What is the pharmacological treatment for GERD?

A

H2 receptor antagonist
proton pump inhibitor
antacids
-may cause rebound acidity but still a good choice to try

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17
Q

Describe H2 receptor antagonists.

A

bind to H2 receptors in gastric parietal cells, reducing H+/K+ ATPase activity
used to treat GERD, peptic ulcers (duration not as long as PPI)
examples: ranitidine, famotidine, cimetidine, nizatidine

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18
Q

Describe proton pump inhibitors.

A

bind to H+/K+ ATPase of the gastric parietal cell, thereby preventing acid secretion (blocks H2 and muscarinic receptor)
used to treat GERD, peptic ulcers, H.pylori-related ulcers, duodenal ulcers and Zollinger-Ellison disorder (acid hypersecretion)
examples: pantoprazole, omeprazole, rabeprazole, esomeprazole, lansorprazole, dexlansoprazole

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19
Q

What is the role of parietal cells? What about ECL cells?

A

parietal cells: secrete acid into the stomach
ECL cells: secrete histamine and peptide hormones

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20
Q

Describe what happens when ECL cells and parietal cells are stimulated.

A

ECL cells and parietal cells both have muscarinic receptors (target for ACh)
when ECL cells are stimulated by ACh, they secrete histamine which stimulates parietal cells to secrete acid
when the parietal cell is stimulated via both its muscarinic receptor and its H2 receptors it secretes acid

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21
Q

What is gastritis?

A

infection or inflammation of the stomach
can be acute or chronic

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22
Q

What is the etiology of gastritis?

A

infection: H. pylori infection is associated with gastric ulcers
irritation: foods (spicy or acidic)
medications: NSAIDs (by blocking Pg synthesis they reduce production of protective mucous), certain antibiotics
alcohol: direct irritant
atrophy of old age: achlorhydria, reduced acid production, greater risk of infection
major stress: surgery, major burns, severe illness
autoimmune (pernicious anemia with B12 deficiency)

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23
Q

What are the signs and symptoms of gastritis?

A

pain
bloating
burning sensation
heavy feeling in stomach
belching or flatulence
nausea/vomiting
loss of appetite
weight loss (chronic)
blood in vomit or stool (coffee-ground emesis, melena)

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24
Q

How is gastritis managed for its associated etiology?
infection
irritation
medications
alcohol
major stress
autoimmune

A

infection: triple antibiotic therapy + PPI
irritation: avoid trigger foods, use H2 antagonist, antacid
medications: NSAIDs or certain antibiotics taken with food
alcohol: avoid excessive use and smoking + alcohol
major stress: H2 antagonist, PPI
autoimmune: manage symptoms and deficiency

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25
What do gastric ulcers put someone at risk for?
bleeding, blood loss-->anemia
26
What is the treatment for gastric ulcers?
1. one or two antibiotics (amoxicillin, tetracycline, metronidazole or clarithromycin) 2. and bismuth 3. and H2 antagonist or PPI *2-3 weeks of treatment, surgery only if perforated or nonhealing*
27
What are the countries with higher rates of gastric cancer often associated with higher rates of?
diets high in salt and smoked foods higher rates of H pylori
28
What are the risk factors for gastric cancer?
infections: H. pylori, Epstein-Barr virus genetic factors prior stomach surgery or radiation exposure rubber industry work smoking, alcohol, high salt diet being overweight precancerous lesions: gastric epithelial dysplasia and gastric adenoma
29
True or false: ulcers should be investigated and treated early to identify if gastric cancer is present
true
30
What are the systemic symptoms of gastric cancer?
fatigue weight loss anemia lymph node involvement vomiting pain abdominal fullness/bloating blockage
31
What type of tumors are most cases of gastric cancers?
most common: adenocarcinoma less common: lymphoma, leiomyosarcoma, neuroendocrine
32
What is the treatment for gastric cancer?
early stage: surgery later stages: radiation and chemotherapy
33
What are the three parts of the pancreas?
tail body head
34
What are the exocrine functions of the pancreas?
produce bicarbonate and digestive enzymes such as lipase amylase and protease to break down fats, carbohydrates, and proteins
35
How does pancreatic fluid enter the duodenum?
through papilla (major and minor) near the common bile duct
36
What can cancer of the head of the pancreas lead to?
it can impinge on the duodenum and ducts leading to digestive problems
37
What is acute pancreatitis?
acinar cell injury and duct obstruction results inappropriate extracellular leakage of activated digestive enzymes and thus autodigestion of pancreatic and extra-pancreatic tissues spectrum of severity: self-limiting to fatal hemorrhagic pancreatitis with massive necrosis
38
What are the signs and symptoms of acute pancreatitis?
signs: -serum amylase and lipase become elevated -shock and collapse may occur symptoms: -severe epigastric pain that radiates to the upper back -nausea and vomiting
39
How is acute pancreatitis managed?
supportive care avoid alcohol pain management
40
What are the complications of acute pancreatitis?
half of cases the necrotic pancreas becomes infected with intestinal bacteria which increases risk of death repeated incidence can lead to chronic pancreatitis and fibrosis
41
How does chronic pancreatitis present?
presents as recurrent or persistent epigastric pain with signs of pancreatic insufficiency -poor digestion -pain upon eating -greasy/smelly stools -malnutrition *80% due to alcoholism*
42
What do we mean when we say that alcohol is a pancreatic secretagogue?
it stimulates secretion however these extra proteins can clog up the pancreatic ducts leading to obstructions
43
What might individuals be put on as their pancreatic function declines?
pancreatic enzyme supplements (pancreatin)
44
What are the causes of pancreatitis?
alcohol abuse (especially binge drinking) gallstones (mechanical obstruction) medications (multiple mechanisms) infections (parasitic, fungal, worms) other/idiopathic (cystic fibrosis, ischemia, trauma, autoimmune)
45
Differentiate between acute pancreatitis and chronic pancreatitis.
acute: -can occur suddenly and goes away within a few days -most often cause by gallstones or heavy alcohol use, sometimes no cause can be found -most cases are mild -most involve a short hospital stay chronic: -takes many years to develop and does not go away, permanent injury or scarred -associated with frequent flare-ups or persistent symptoms such as pain -many patients have calcifications of the pancreas (CT scan) -most patients have a good outlook if they follow their management plan
46
What does the enteric nervous system and gastrointestinal hormones control?
GI motility and secretions
47
What factors will slow gastric emptying? What factors will speed up gastric emptying?
slow: -fed state -high fat foods -supine fast: -fasted state -high carbohydrate liquid
48
True or false: the small intestine is more variable in terms of transit time than the large intestine and stomach
false less variable, 2-6hrs of transit time
49
Which part of the GI tract has a highly variable transit time? What are the factors that influence its transit time?
the colon influenced by: -diet composition (high vs low fiber) -age (infant: very fast ; elderly: maybe days) -hydration status -fed vs fasted
50
Describe gastrin.
peptide hormone from G cells of the stomach and duodenum stimulates acid secretion after food intake stimulates secretion of other hormones such as pepsinogen, intrinsic factor and secretin increases intestinal motility and gastric motility
51
What is autoimmune gastritis?
attack on G cells that produce gastrin resulting in less acid production negative effect on digestion and increases susceptibility to infection
52
Describe secretin.
comes from the duodenum and ileum stimulates secretion of water and bicarbonate from the pancreas reduces motility and inhibits gastrin
53
Describe cholecystokinin.
stimulates secretion of pancreatic enzymes and causes contraction and emptying of the gallbladder fatty meal will result in CCK stimulation and release of bile into the small intestine
54
Describe somatostatin.
from the stomach and pancreas inhibits secretion and actions of many hormones
55
Describe motilin.
increases gastric emptying and small intestine motility
56
What are examples of intestinal vascular diseases?
hemorrhoids (swollen vein or group of veins in the region of the anus) ischemic bowel disease chronic ischemia acute thrombosis of mesenteric arteries and veins (blood clot) nonocclusive intestinal infarcts (tissue death) hernia can strangulate tissue and cause ischemia
57
Differentiate between diarrhea and constipation.
diarrhea: -excessive motility -loss of fluids and potential for dehydration -chronic can lead to malabsorption -commonly due to infectious or toxic agents due to epithelial disruption (drugs, food, chemo) -treatment: rehydration, bulking agents, anti-motility drugs constipation: -inadequate motility (acute/chronic) -stool becomes harder and more difficult to pass -impactions -discomfort -enteric nervous system disruption -treatments: motility agents (sennosides bisacodyl, PEG), fluids, bulking agents, stool softeners (docusate)
58
Who are the people at risk for diarrhea?
travelers children in daycare elderly in nursing homes food workers hospitalized patients
59
What are the bacteria that commonly cause food poisoning? What is the treatment for food poisoning?
campylobacter jejuni, salmonella supportive care, antibiotics only needed if systemic illness occurs
60
True or false: infectious diarrhea is commonly associated with travel or are food-borne
true
61
What are the bacteria that most commonly cause infectious diarrhea?
salmonella campylobacter shigella shiga toxin-producing E.coli
62
Differentiate between noninflammatory and inflammatory infectious diarrhea.
noninflammatory: -usually less severe but can cause dehydration -E.coli, clostridium, S. aureus, rotavirus, norovirus, Giardia inflammatory: -bloody diarrhea and presence of fecal leukocytes -more severe -salmonella, shigella, campylobacter, STP E.coli, C. diff
63
Describe the management of diarrhea.
self-management: -rehydration -rest -loperamide to reduce duration of symptoms -simethicone for gas and cramping -hygiene to reduce transmission to others -heathy diet refer to physician: -bloody diarrhea - >7 days -travel associated -immunocompromised -fever, severely ill, debilitated -complex patient -very young or very old
64
What are the causes of intestinal obstruction?
paralytic ileus mechanical (obstructive) ileus -atresia or stenosis -stricture -intussusception -volvulus -hernia -adhesions -neoplasms
65
What is the third most common cancer of internal organs?
intestinal neoplasms
66
What is inflammatory bowel disease?
chronic inflammation of portions of the GI tract caused by a combination of genetics, environment, and immune response
67
What are the complications of IBD?
malnutrition and malabsorption anemia perforated bowel colon cancer intestinal fistulas ruptures osteoporosis
68
What are the two main forms of IBD?
Crohns disease ulcerative colitis
69
True or false: IBD is diagnosed in adolescence or early adulthood
true
70
What are some of the extraintestinal symptoms that some IBD patients will experience?
arthritis certain eye conditions fever aphthous ulcers
71
What are the additional risk factors for IBD?
smoking family history fatty diet hormonal medications stress environmental pollution urban residence
72
What are the symptoms of IBD?
abdominal pain mouth/stomach ulcers diarrhea rectal bleeding loss/change in appetite fever weight loss fatigue change/loss of menstrual cycle
73
What is the etiology for Crohns disease?
unknown infectious and immunologic mechanisms have been proposed
74
What does the distribution of bowel involvement appear as in Crohns disease?
irregular with more normal intervening "skip" areas
75
Where is ulcerative colitis restricted to?
colon
76
What is the peak age for ulcerative colitis?
18-35
77
What are the symptoms of ulcerative colitis?
*gradual onset, can be very debilitating* redness swelling pain loss of function diarrhea (maybe bloody) urgency
78
Differentiate between Crohns and ulcerative colitis based on the following: familial, peak age, immune disturbances, extraintestinal complications, treatment, distribution, transmural, granuloma, fistula, megacolon, cancer
familial: Crohns ++, UC ++ peak age: Crohns=15-25, UC=15-25 immune disturbances: Crohns +, UC + extraintestinal complications: Crohns +, UC + tx: Crohns +, UC + distribution: Crohns=segmental including ileum, UC=diffuse, only colon transmural: Crohns ++, UC - granuloma: Crohns +, UC - fistula: Crohns +, UC - megacolon: Crohns -, UC + cancer: Crohns +, UC ++
79
What are the five types of medications used to treat IBD?
aminosalicylates (anti-inflammatory) -mesalamine, balsalazide, olsalazine corticosteroids (anti-inflammatory) -prednisone, hydrocortisone immunomodulators (suppress immune system) -azathioprine antibiotics biologics (mod-severe cases) -adalimumab, infliximab
80
Describe the different biologics for IBD.
anti-TNF: -TNF a one of the signals involved in inflammation in IBD -adalimumab and infliximab a4B7 integrin blockers: -block attachment of WBC to tissues, preventing entry -vedolizumab antibody to p40 subunit of IL-12 and IL-13: -IL12 and 13 are messengers that recruit WBCs -ustekinumab, risankizumab
81
How do we monitor biologic therapy for IBD?
measuring levels of biologic in blood and sometimes measuring antibodies against the biologic fecal calprotectins: -measurements in stool -high if there is intestinal inflammation, low if biologic is efficacious

PHAR123 (15 decks)

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