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ALU 201 > Chapter 1 > Flashcards

Chapter 1 Flashcards

1
Q

Food is passed to the esophagus through the ________ ______process of swallowing.

A

Neurologically mediated process

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2
Q

Once food enters the esophagus, how is it forced downward?

A

By gravity and rhythmic contractions (peristalsis) if the muscles that make up the outer two layers of the esophagus.

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3
Q

What is the name for the rhythmic contractions that push fois from the esophagus to the stomach?

A

Peristalsis

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4
Q

What is another name for the gastroesophageal junction (GE junction)?

A

Z-line

Because of it’s zigzag appearance

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5
Q

What is the major function of the stomach?

A

To continue the mechanical grinding of the food bolus and to enhance the chemical process of digestion

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6
Q

How is the chemical process of digestion done

A

Through hydrochloride acid (HCL) and pepsin.

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7
Q

Does the stomach absorb nutrients?

A

Not for the most part, but it does absorb alcohol

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8
Q

What is the other role of the stomach?

A

Production of intrinsic factor, a protein that is necessary for the absorption of vitamin B12.

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9
Q

Where is food passed after stomach

A

Through pylorus

Into first part of small intestine (duodenum)

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10
Q

Where are digestive enzymes produced

A

Pancreas

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11
Q

Where is bile produced

A

Liver

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12
Q

Bile and digestive enzymes empty into the duodenum through a common opening known as the _________

A

Ampulla or papilla of Vater

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13
Q

As nutrients pas through the rest of the small intestine, they are absorbed through multiple projections of the mucosa called the ____

A

Villi

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14
Q

How long is the small intestine

A

Average 22 feet

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15
Q

Where does the residual solution that is not absorbed by the small intestine go

A

Passes through the ileocecal valve into the cecum

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16
Q

The last 15 cm of the colon is called the _____

A

Rectum

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17
Q

The structure that controls the fecal outflow is called the ___\

A

Anus

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18
Q

What is the major function of the large intestine

A

Reabsorb water and electrolytes passing from the small intestine and to control the elimination of the digestive waste material

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19
Q

The large bowel is host to many bacteria that aid in the production of ______

A

Vitamin K

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20
Q

Oral cancer is usually what type

A

SCC and it tends to recur and has high mortality rate

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21
Q

What is the name for pain that is associated with dysphasia

A

Odynophagia

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22
Q

What is esophageal manometry

A

Pressure monitoring of the esophagus

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23
Q

What meds are often used to treat primary motor disorder (e.g. Esophageal spasm)

A

Metoclopramide/reglan
Nifedipine/procardia
NTG

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24
Q

What is achalasia

A

Failure of the lower esophageal sphincter to relax, resulting in significant dilatation if the esophagus

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25
Q

What is name for heartburn

A

Pyrosis

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26
Q

What is metaplasia and Barrett’s

A

Chronic inflammation such as from GERD can cause a transition of the normal squamous esophageal mucosa into glandular gastric mucosa. Further changes to the mucosa (metaplasia) a using it to resemble intestinal cells (intestinal Izard on) is Barrett’s esophagus

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27
Q

How does Barrett’s appear endoscopically

A

Pink areas of mucosa in an esophagus that is a pearly white color

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28
Q

Barrett’s - over time, the newly transformed, intestinalized cells become dysplastic. what does dysplastic mean?

A

pre-malignant, and the dysplasia can be low grade or high grade

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29
Q

how can Barrett’s be treated

A

radio frequency ablation and photodynamic therapy, but would still require close surveillance to watch for recurrence

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30
Q

what is the most common surgery for GERD

A

Nissan fundoplication (laparoscopic)

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31
Q

is SCC or adenocarcinoma from Barrett’s more common?

A

SCC used to be the most common, but now adenocarcinoma from Barrett’s has become more common.

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32
Q

is the mortality rate from esophageal cancers low or high?

A

high

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33
Q

describe esophageal hernia

A

stomach normally lies in and cavity with gastroesophageal junction being just below the level of the diaphragm. when the stomach pushes up through the diaphragm into the chest, it is called esophageal or hiatal hernia

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34
Q

what % of gastric ulcers are malignant

A

about 1%

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35
Q

what type of lymphoma can h pylori be associated with

A

MALT - mucosa-associated lymphoid tissue lymphoma

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36
Q

what does the pancreas produce

A

insulin and pancreatic enzymes

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37
Q

what are the possible causes of pancreatitis

A

alcohol, blockage by gallstones (gallstone pancreatitis), meds, infection, autoimmune disease, hyperTG with TG levels >1000, and idiopathic.

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38
Q

does acute pancreatitis have high or low mortality rate?

A

high

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39
Q

how is pancreatitis diagnosed

A

elevated serum amylase
elevated lipase
ultrasound, CT, MRI, MRCP

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40
Q

what other problems can chronic pancreatitis cause

A

inadequate insulin production (diabetes)

inadequate digestive enzyme production (pancreatic insufficiency)

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41
Q

name 2 meds for pancreatic insufficiency

A

Creon, pancrease (oral digestive enzymes)

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42
Q

name 3 categories of pancreatic tumors (solid)

A

benign, malignant, hormone-producing (endocrine)

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43
Q

what is most common pancreatic tumor

A

pancreatic adenocarcinoma, with very high mortality rate

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44
Q

what are the 3 most common pancreatic endocrine tumors

A

gastronomes (collinger-ellison syndrome, cause ulcers)
insulinomas (cause hypoglycemia)
vasoactive intestinal peptide producing tumors (VIPomas) that cause watery diarrhea

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45
Q

what tests are done to determine if a pancreatic cystic lesion is benign or malignant

A

ERCP, CT, MRI

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46
Q

what pancreatic cystic lesions of no malignant potential

A

pseudocyst, lymphoepithelial cyst, retention cyst, congenital cyst, cystic lymphangioma, cavernous hemangioma, serous cystic adenoma

47
Q

what pancreatic cystic lesions have malignant potential

A

intraductal papillary mutinous neoplasm, mutinous cystic neoplasm,
intraductal tubular carcinoma

48
Q

what pancreatic cystic lesions are malignant

A

cystic ductal adenocarcinoma, cystic neuroendocrine tumor, solid pseudo papillary neoplasm, cystic pancreatoblastoma, cystic acinar cystoadenocarcinoma, mature cystic teratoma

49
Q

what are the causes of inadequate absorption of nutrients

A

insufficient breakdown of food (pancreatic insufficiency)
disruption of the intestinal lining
too rapid of passage of food through the intestines

50
Q

in what disease is disruption or destruction of the villous surface of the small intestine seen

A

celiac disease

51
Q

what is Chron’s disease and what is another name for it

A

also known as granulomatous or regional enteritis.
inflammatory process that can affect any part of the GI tract but most commonly the distal third of the small intestine (ileum) and the colon. possible autoimmune basis.

52
Q

what part does ulcerative colitis affect

A

only the large intestine

53
Q

which always involves the rectum - chron’s or UC?

A

UC always involves the rectum and is continuous to some proximal part of the large intestine.

54
Q

which can have skip lessons - UC or Chron’s?

A

Chron’s can affect the bowel in a non-continuous pattern, creating skip lesions, with areas of severe inflammation with intervening normal mucosa

55
Q

which has increased risk of colon cancer- chron’s, UC or both?

A

Both.

56
Q

how many years after onset of Chron’s or UC is there steady, significant, increased risk of developing cancer?

A

8-10 years

57
Q

what other factor is risk of colon cancer dependent upon

A

extent of disease (how far up colon it has spread)

58
Q

ulcerative proctitis can go how far up the colon?

A

distal 15 cm, which is limited to rectum

59
Q

how far up colon can ulcerative proctosigmoiditis go

A

up 10 25 cm

60
Q

do ulcerative proctitis and ulcerative proctosigmviditis have smaller or larger cancer risk

A

small increased cancer risk

61
Q

what is the etiology of chron’s

A

unknown. possibly autoimmune

62
Q

how often should someone with chron’s x 10 to more years have colonoscopy?

A

every 1-2 years

63
Q

if scope for chron’s finds dysplasia what is treatment

A

total colectomy, which is not curative for chron’s

64
Q

what are meds for chron’s

A

abx, steroids, immunosuppressive agents such as imuran, sulfasalazine, with goal to put into remission

65
Q

what are meds for UC

A

abx, sulfasalazine, pentasa, asacol, canasa, rowasa, steroids, DMARDs used to avoid prolonged need for steroids

66
Q

From underwriting perspective, what is chron’s disease mortality associated with?

A

bleeding, malabsorption, complications of the meds used to treat the disease, late cancer risk, obstructive, infectious, and surgical complications

67
Q

From underwriting perspective, what is UC mortality associated with?

A

risk of acute disease causing bleeding, acute dilatation (toxic megacolon), and perforation of colon. when acute symptoms are not severe, mortality most significantly affected by the increased risk of cancer

68
Q

what extra intestinal complications are associated with chron’s and UC

A

ankylosing spondylitis, arthritis, iritis, pyoderma gangrenous, erythema nodosum

69
Q

elevated LFTs from Chron’s are felt to be secondary to what?

A

nonspecific inflammation around the microscopic bile ducts, and felt to be of little clinical significance

70
Q

abnml LFTs from UC can be result of what, and what is the risk

A

usually Alk phos and GGT
can be primary sclerosing cholangitis (PSG)
bile ducts become scarred and narrowed, obstructing bile flow, eventually leading to cirrhosis and death
this persists even after colectomy

71
Q

is rectal bleeding more common with UC or Chron’s

A

UC - common

chron’s - occassional

72
Q

is abdominal pain more common with UC or Chron’s

A

UC- uncommon

Chron’s - common

73
Q

is rectal involvement more common with UC or Chron’s

A

UC- almost 100%

chron’s - 50%

74
Q

is fistula formation more common with UC or Chron’s

A

UC - No

Chron’s - common

75
Q

is stricture, obstruction more common with UC or Chron’s

A

UC - No

Chron’s- common

76
Q

is perianal, perirectal abscess more common with UC or Chron’s

A

UC - uncommon

chron’s - common

77
Q

what type of involvement is there with UC vs Chron’s

A

UC - continuous

chron’s - discontinuous (skip areas)

78
Q

what is the depth of involvement with UC vs chron’s

A

UC - mucosa and submucosa

chron’s - transmural

79
Q

is bowel involvement more common with UC or Chron’s

A

UC - not involved

chron’s - often involved

80
Q

is there greater risk of malignancy with UC or chron’s

A

UC.- greatly increased

chron’s - moderately increased

81
Q

what is IBD

A

Chron’s and UC

82
Q

IBS

A

disorder of the motor function of the GI tract, creating areas of spasm and pain. doesn’t cause inflammation, bleeding, or obstruction

83
Q

what are the symptoms of IBS

A

diarrhea, abd pain, bloating and/or constipation. psychological stress can influence

84
Q

what symptoms don’t appear with IBS

A

almost never any weight loss, usually doesn’t occur during sleep

85
Q

what tests can dx IBS?

A

none so far. dx of exclusion

86
Q

what is treatment for IBS

A

fiber, antispasmodics, antidiarrheal agents and/or anticonstipation agents

87
Q

what is the risk with IBS

A

no mortality risk

can be significant morbidity issues

88
Q

which part of the GI tract is most often affected by neoplasms?

A

large intestine

89
Q

describe types of colon polyps (shapes)

A

sessile - broad-based

pedunculate - on a stalk

90
Q

what determines the malignancy potential of a colon polyp

A

the histology

91
Q

type of pre-malignant polyps

A

adenomas (tubular adenomas, villouss adenomas, tubulovillous adenomas)
serrated polyps or serrated adenomas

92
Q

are adenomas low or high grade in dysplasia

A

low-grade dysplastic, but the larger or more villous the polyp is, the higher the malignant potential

93
Q

what term describes benign polyps with no malignant potential

A

hyperplastic, inflammatory, or juvenile polyps

94
Q

polyposis syndromes

A

FAP, Gardner’s syndrome, Turcot syndrome, MYH polyposis, HNPCC or Lynch syndrome, Peutz-Jeghers syndrome, juvenile polyposis

95
Q

colon polyps and cancer occur more frequently after what age?

A

50

96
Q

what age does colonoscopy screening start?

A

age 50 for avg risk individuals

age 40 for those with family hx of colon polyps

97
Q

what is the repeat colonoscopy interval

A

in 3-5 yrs if hx of premalignant polyps or family hx

in 8-10 yrs for all others

98
Q

describe in situ vs invasive colon cancer and where mets most frequently occur

A

in situ is confined to the superficial layer of the bowel
invasive spreads beyond that
mets most frequently to liver, lung, brain

99
Q

where do diverticula most commonly occur

A

lt side of the colon

100
Q

what are the most common sources of large volume upper GI bleed

A

esophageal varices, ulcers, severe gastritis, mallory-weirs tear (tear of lower esophagus usually after vomiting)

101
Q

large volume lower GI bleeding (hematochezia) is most commonly caused by:

A

diverticulosis, AVMs, polyps, cancers

102
Q

what are the mortality risks with GI bleed

A

mortality is a/w the underlying cause, acute complications a/w rapid blood volume loss ( syncope, shock, and MI), and risks of the therapy needed to control and treat bleeding (surgery and transfusions). the cause of the bleeding is the key to determining mortality risk.

103
Q

what is the major impairment of concern in older age groups

A

colon cancer

104
Q

what is the major impairment of concern is younger age groups

A

inflammatory causes and they concomitant mortality risk

105
Q

what are the causes of intestinal obstruction

A
  • blockages in small or large intestine by tumors, polyps or foreign bodies
  • bowel twisting on itself (volvulus)
  • adhesions from prior surgery or prior intrabdominal infection causing tethering of the bowel and obstruction
  • telescoping of the bowel on itself (intussusception)
  • herniation of the bowel through the abd wall, inguinal ligament or diaphragm
    (last 4 can also cut off blood supply to the intestine and result in ischemia or infarction with gangrene and risk of perforation)
106
Q

what is intestinal ischemia

A

disruption of blood flow to the intestines

107
Q

what are the causes of intestinal ischemia

A

adhesions, intussusception, herniation, volvulus, clotting of intestinal arteries d/t atherosclerosis, clot or embolism. sudden drop in BP can also result in ischemia of the bowel

108
Q

is bariatric surgery usually done laparoscopically or open?

A

laparoscopically

109
Q

what is the weight reduction typical after bariatric surgery

A

45-80% of excess weight loss, corresponding to 60-120 lbs over 12-18 months with bypass or 24 months with gastrectomy/lap band, with 10% regain over time

110
Q

what is the mortalityy risk with bariatric surgery

A

small post mortality of <0.5%

111
Q

what are possible long term probs after bariatric surgery

A

esophageal reflux, stenosis of the anastomosis sites, ulceration, bleeding, vitamin and mineral deficiencies, intestinal obstruction

112
Q

what obesity related illness improve or resolve after bariatric surgery and after how long?

A

DM2, HTN, HLD, NAFLD, OSA, within first 12 months. cancer rates also decrease long term after surgery

113
Q

what is the long term overall decrease in mortality after bariatric surgery?

A

mortality improves 40% by 7 years and persists up to 20 years when compared to those who didn’t have the surgery

ALU 201 (20 decks)

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