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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
Q

What do gastric ulcers put someone at risk for?

A

bleeding, blood loss–>anemia

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26
Q

What is the treatment for gastric ulcers?

A
  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
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27
Q

What are the countries with higher rates of gastric cancer often associated with higher rates of?

A

diets high in salt and smoked foods
higher rates of H pylori

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28
Q

What are the risk factors for gastric cancer?

A

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

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29
Q

True or false: ulcers should be investigated and treated early to identify if gastric cancer is present

A

true

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30
Q

What are the systemic symptoms of gastric cancer?

A

fatigue
weight loss
anemia
lymph node involvement
vomiting
pain
abdominal fullness/bloating
blockage

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31
Q

What type of tumors are most cases of gastric cancers?

A

most common: adenocarcinoma
less common: lymphoma, leiomyosarcoma, neuroendocrine

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32
Q

What is the treatment for gastric cancer?

A

early stage: surgery
later stages: radiation and chemotherapy

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33
Q

What are the three parts of the pancreas?

A

tail
body
head

34
Q

What are the exocrine functions of the pancreas?

A

produce bicarbonate and digestive enzymes such as lipase amylase and protease to break down fats, carbohydrates, and proteins

35
Q

How does pancreatic fluid enter the duodenum?

A

through papilla (major and minor) near the common bile duct

36
Q

What can cancer of the head of the pancreas lead to?

A

it can impinge on the duodenum and ducts leading to digestive problems

37
Q

What is acute pancreatitis?

A

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
Q

What are the signs and symptoms of acute pancreatitis?

A

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
Q

How is acute pancreatitis managed?

A

supportive care
avoid alcohol
pain management

40
Q

What are the complications of acute pancreatitis?

A

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
Q

How does chronic pancreatitis present?

A

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
Q

What do we mean when we say that alcohol is a pancreatic secretagogue?

A

it stimulates secretion
however these extra proteins can clog up the pancreatic ducts leading to obstructions

43
Q

What might individuals be put on as their pancreatic function declines?

A

pancreatic enzyme supplements (pancreatin)

44
Q

What are the causes of pancreatitis?

A

alcohol abuse (especially binge drinking)
gallstones (mechanical obstruction)
medications (multiple mechanisms)
infections (parasitic, fungal, worms)
other/idiopathic (cystic fibrosis, ischemia, trauma, autoimmune)

45
Q

Differentiate between acute pancreatitis and chronic pancreatitis.

A

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
Q

What does the enteric nervous system and gastrointestinal hormones control?

A

GI motility and secretions

47
Q

What factors will slow gastric emptying? What factors will speed up gastric emptying?

A

slow:
-fed state
-high fat foods
-supine
fast:
-fasted state
-high carbohydrate liquid

48
Q

True or false: the small intestine is more variable in terms of transit time than the large intestine and stomach

A

false
less variable, 2-6hrs of transit time

49
Q

Which part of the GI tract has a highly variable transit time? What are the factors that influence its transit time?

A

the colon
influenced by:
-diet composition (high vs low fiber)
-age (infant: very fast ; elderly: maybe days)
-hydration status
-fed vs fasted

50
Q

Describe gastrin.

A

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
Q

What is autoimmune gastritis?

A

attack on G cells that produce gastrin resulting in less acid production
negative effect on digestion and increases susceptibility to infection

52
Q

Describe secretin.

A

comes from the duodenum and ileum
stimulates secretion of water and bicarbonate from the pancreas
reduces motility and inhibits gastrin

53
Q

Describe cholecystokinin.

A

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
Q

Describe somatostatin.

A

from the stomach and pancreas
inhibits secretion and actions of many hormones

55
Q

Describe motilin.

A

increases gastric emptying and small intestine motility

56
Q

What are examples of intestinal vascular diseases?

A

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
Q

Differentiate between diarrhea and constipation.

A

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
Q

Who are the people at risk for diarrhea?

A

travelers
children in daycare
elderly in nursing homes
food workers
hospitalized patients

59
Q

What are the bacteria that commonly cause food poisoning? What is the treatment for food poisoning?

A

campylobacter jejuni, salmonella
supportive care, antibiotics only needed if systemic illness occurs

60
Q

True or false: infectious diarrhea is commonly associated with travel or are food-borne

A

true

61
Q

What are the bacteria that most commonly cause infectious diarrhea?

A

salmonella
campylobacter
shigella
shiga toxin-producing E.coli

62
Q

Differentiate between noninflammatory and inflammatory infectious diarrhea.

A

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
Q

Describe the management of diarrhea.

A

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
Q

What are the causes of intestinal obstruction?

A

paralytic ileus
mechanical (obstructive) ileus
-atresia or stenosis
-stricture
-intussusception
-volvulus
-hernia
-adhesions
-neoplasms

65
Q

What is the third most common cancer of internal organs?

A

intestinal neoplasms

66
Q

What is inflammatory bowel disease?

A

chronic inflammation of portions of the GI tract
caused by a combination of genetics, environment, and immune response

67
Q

What are the complications of IBD?

A

malnutrition and malabsorption
anemia
perforated bowel
colon cancer
intestinal fistulas
ruptures
osteoporosis

68
Q

What are the two main forms of IBD?

A

Crohns disease
ulcerative colitis

69
Q

True or false: IBD is diagnosed in adolescence or early adulthood

A

true

70
Q

What are some of the extraintestinal symptoms that some IBD patients will experience?

A

arthritis
certain eye conditions
fever
aphthous ulcers

71
Q

What are the additional risk factors for IBD?

A

smoking
family history
fatty diet
hormonal medications
stress
environmental pollution
urban residence

72
Q

What are the symptoms of IBD?

A

abdominal pain
mouth/stomach ulcers
diarrhea
rectal bleeding
loss/change in appetite
fever
weight loss
fatigue
change/loss of menstrual cycle

73
Q

What is the etiology for Crohns disease?

A

unknown
infectious and immunologic mechanisms have been proposed

74
Q

What does the distribution of bowel involvement appear as in Crohns disease?

A

irregular with more normal intervening “skip” areas

75
Q

Where is ulcerative colitis restricted to?

A

colon

76
Q

What is the peak age for ulcerative colitis?

A

18-35

77
Q

What are the symptoms of ulcerative colitis?

A

gradual onset, can be very debilitating
redness
swelling
pain
loss of function
diarrhea (maybe bloody)
urgency

78
Q

Differentiate between Crohns and ulcerative colitis based on the following:
familial, peak age, immune disturbances, extraintestinal complications, treatment, distribution, transmural, granuloma, fistula, megacolon, cancer

A

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
Q

What are the five types of medications used to treat IBD?

A

aminosalicylates (anti-inflammatory)
-mesalamine, balsalazide, olsalazine
corticosteroids (anti-inflammatory)
-prednisone, hydrocortisone
immunomodulators (suppress immune system)
-azathioprine
antibiotics
biologics (mod-severe cases)
-adalimumab, infliximab

80
Q

Describe the different biologics for IBD.

A

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
Q

How do we monitor biologic therapy for IBD?

A

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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